For decades, epidemiologists and social scientists have documented the connection between inequality and infectious disease. People’s risk of exposure can depend on where they live, how many people share their home, whether they can work remotely, and how easily they can reach a clinic. Access to vaccines, testing, treatment, transportation, and paid sick leave can further shape the course of an outbreak. At the same time, mathematical epidemiologists have built increasingly sophisticated models to forecast transmission and evaluate public-health interventions. Yet the social causes of unequal risk have often remained separate from the formal machinery used to model epidemics.

A new study in Biology Letters seeks to close that gap with a metric called structural causal influence, or SCI. The framework is designed for use with standard disease-transmission models and quantifies how strongly social determinants of health alter the behavior of an epidemic. Rather than treating inequality as background information, SCI allows researchers to represent factors such as crowded housing, limited vaccine access, financial constraints, and unequal healthcare availability as mechanisms that can directly change transmission and disease outcomes.

The approach is built around a central distinction in causal science: observing that two conditions occur together is not the same as showing that one helps produce the other. A disadvantaged community may experience higher infection rates because of multiple overlapping factors, including increased exposure, delayed access to care, or reduced ability to isolate. SCI is intended to help identify the influence of such structural conditions within a mathematical model. By comparing how the model behaves when a social factor is present, altered, or removed, researchers can estimate how that factor changes the spread of infection and the likely effect of an intervention.

The researchers tested the concept using canonical models such as SIR, which divides a population into susceptible, infected, and removed groups. In its simplest form, an SIR model describes how individuals move between these categories as infection spreads and recovery or removal occurs. The model’s basic parameters include the rate at which susceptible people encounter infectious individuals and the rate at which infected people recover or are otherwise removed from transmission. Although such models are deliberately streamlined, they can be extended to represent multiple communities, different contact patterns, unequal access to vaccination, and varying levels of healthcare capacity.

That added structure matters because a population-wide average can conceal the conditions in a smaller, high-risk group. Modeling with SCI showed that an epidemic may develop even when the overall transmission risk appears low. If infection spreads efficiently within a disadvantaged subgroup, that group can sustain transmission despite a reassuring average for the population as a whole. Depending on the connections between groups, infections may then spill into the wider community. A low average risk, in other words, does not necessarily mean that every population segment is protected from sustained outbreak dynamics.

This result has important implications for the interpretation of familiar epidemic indicators. Measures such as an average reproduction number summarize transmission across a population, but they can obscure differences in contact rates, susceptibility, vaccination coverage, or access to treatment. A single value may therefore suggest that an outbreak is under control while transmission remains intense in a particular neighborhood, institution, or occupational group. SCI offers a way to examine how those differences contribute to the overall dynamics and whether reducing them would change the trajectory of the epidemic.

The framework also provides a tool for evaluating public-health choices. An intervention that appears inefficient when judged only by its immediate effect on the population average may have a larger indirect benefit if it protects a group that is sustaining transmission. Increasing vaccine access in underserved communities, improving ventilation in crowded settings, expanding hospital capacity, or reducing financial barriers to testing and isolation could affect both direct health outcomes and the broader network of transmission. The metric is intended to help decision-makers compare these effects and determine where limited resources may produce the greatest reduction in disease spread.

The authors deliberately chose interpretable mathematical models rather than embedding the metric in complex artificial-intelligence systems. Neural networks can identify patterns in large datasets, but their internal reasoning may be difficult to inspect, making it harder to determine why a prediction was produced or which social conditions shaped it. By working with models that researchers and policymakers can read, SCI is designed to make assumptions visible and causal relationships easier to examine. The same principle could allow the framework to be adapted beyond acute epidemics, including studies of chronic disease, pollution, and climate-related health risks.

Brandon Ogbunu of the Santa Fe Institute and Yale University, the study’s senior author, says the findings reinforce the idea that infectious-disease control cannot be separated from equity. Sam Scarpino of Northeastern University, a co-author and Santa Fe Institute External Professor, describes the work as an example of how epidemiology, statistics, and data science can be combined to address questions that no single discipline can resolve alone. The researchers argue that directing more protection and healthcare resources toward communities facing the greatest structural disadvantages is not only a matter of fairness. Because outbreaks move through connected populations, reducing transmission in those communities can ultimately help protect everyone.

Subject of Research: Social inequality and its causal influence on infectious-disease transmission models

Article Title: Structural causal influence (SCI) captures the forces of social inequality in models of infectious disease

News Publication Date: 19 August 2026

Web References: https://santafe.edu/people/profile/ogbunu-brandon ; https://www.santafe.edu/people/profile/sam-scarpino

References: Biology Letters, “Structural causal influence (SCI) captures the forces of social inequality in models of infectious disease,” publication date: 19 August 2026

Image Credits: Edson De la O / Santa Fe Institute

Keywords: infectious disease, viral transmission, epidemic modeling, social inequality, health disparities, structural causal influence, SCI, SIR model, public health, vaccination access, healthcare access, epidemiology, computational biology

Mutation is the raw material of evolution. Every generation, errors can occur when DNA is copied, repaired or rearranged. Most mutations are neutral or harmful, but a small number can alter traits in ways that affect survival and reproduction. The frequency at which these changes appear is known as the mutation rate, and it helps determine how quickly populations can respond to environmental pressures. A high mutation rate may supply genetic variation rapidly, while a low rate can preserve highly successful genetic combinations over long periods. Yet mutation rates are not fixed properties shared equally by all organisms. They can differ among species, populations, tissues and even stages of an organism’s life. The new research will examine whether reproductive mode is a major force shaping that variation.

Sexual reproduction creates offspring through the combination of genetic material from two parents, generally through meiosis and fertilization. This process reshuffles existing variants and can help populations purge harmful mutations or combine beneficial ones. Asexual reproduction, by contrast, produces offspring without the fusion of gametes, often generating genetically similar descendants from a single parent. Self-pollinating plants occupy an intermediate but distinctive position: they reproduce sexually, yet the pollen and ovules may originate from the same individual, limiting the genetic mixing associated with outcrossing. These differences affect population structure, effective population size, selection and the efficiency with which natural selection acts on new mutations. The researchers will test how these evolutionary conditions influence the long-term evolution of mutation rates themselves.

The University of Houston team will focus on Tetrahymena, microscopic freshwater organisms made up of single cells. These ciliates use hair-like structures called cilia to move through water and collect food, but their biology is far more complex than their size suggests. Tetrahymena possess distinct nuclear compartments and unusual life cycles, making them valuable systems for studying genome stability and evolutionary change. Previous work by Azevedo and Zufall found that Tetrahymena has the lowest mutation rate ever recorded in an organism. That finding raises an important biological puzzle. If mutation supplies the variation required for adaptation, how can a lineage with such an exceptionally slow rate of genetic change persist and evolve? The new study will investigate what evolutionary pressures and cellular mechanisms may have produced this extreme genomic stability.

Scientists at the University of Iowa will examine snails, while researchers at the University of Toronto will study mustard plants. Within each group, the investigators will compare closely related organisms that differ primarily in their reproductive strategies. This comparative design is intended to reduce the influence of confounding factors such as body size, generation time, ecological niche and genome architecture. By studying related species under carefully matched conditions, the team can ask whether differences in mutation rates track differences in reproductive mode. The researchers will combine empirical measurements with evolutionary modeling, allowing them to compare observed patterns with predictions about selection, genetic drift and the inheritance of mutation-rate modifiers.

Measuring mutation rates is technically demanding because most new mutations are rare and many are invisible at the level of appearance. A mutation may have no immediate effect on an organism’s growth, behavior or survival, particularly if it occurs in a noncoding region of the genome or is masked by another copy of the gene. Researchers therefore need large numbers of DNA sequences, carefully controlled breeding or culturing designs and statistical methods capable of distinguishing genuine inherited changes from sequencing errors. In organisms with short generation times, scientists can follow mutations across multiple generations. In others, they may compare parent-offspring genomes or use population-level genomic data to estimate how quickly variants accumulate. These approaches will help the collaborators determine not only how many mutations occur, but also when and where they arise.

The project’s theoretical component will be led by Azevedo, who will develop models to connect reproductive biology with the evolution of mutation rates. A central issue is the balance between the benefits and costs of genetic change. Mutations can generate useful variation, but most do not improve fitness and some are strongly damaging. Natural selection may therefore favor mechanisms that reduce copying errors and improve DNA repair. However, in rapidly changing environments, a greater supply of mutations may sometimes help populations discover advantageous traits. Reproductive mode can alter this balance by changing how mutations are exposed to selection, how quickly harmful variants are removed and how efficiently beneficial combinations spread. Modeling these processes across different organisms could reveal general principles that apply from single-celled species to plants and animals.

The researchers emphasize that the work is fundamental evolutionary biology, but its implications extend into medicine. Cancer provides a particularly important example because tumor cells reproduce clonally, a form of asexual expansion, as they divide within the body. Some tumors acquire elevated mutation rates through defects in DNA repair or replication, creating diverse subpopulations within the same mass of cancer cells. This genetic diversity can enable a tumor to survive changes in its environment, including exposure to chemotherapy or targeted drugs. Cells carrying mutations that confer treatment resistance may become more abundant, allowing the cancer to continue growing. Understanding how mutation rates evolve in asexual populations could therefore sharpen scientists’ understanding of tumor progression, although the project is not designed as an immediate clinical trial or treatment-development program.

The same evolutionary logic applies to infectious disease and antibiotic resistance. A microbial population exposed to a drug may contain, or rapidly generate, variants that tolerate the treatment. If those variants reproduce more successfully than susceptible cells, resistance can spread through the population. The speed and direction of that process depend on mutation, selection, population size and the movement of genes among organisms. By comparing mutation-rate evolution in systems with different reproductive modes, the NSF-supported collaboration may help clarify why some populations adapt rapidly while others remain genetically stable. Zufall said the group hopes to identify broad patterns rather than explain only the behavior of its chosen species. “We want to find broad patterns that underlie how populations evolve across all of life,” she said.

Azevedo described the collaboration as powerful because it brings together three experimental scientists working on different biological systems and a theoretician capable of integrating the results into a common framework. The project will not assume that sexual reproduction is universally superior or that asexual reproduction inevitably accelerates evolution. Instead, it will examine the conditions under which each strategy changes the costs and benefits of mutation. The findings could reshape how scientists think about genome stability, adaptation and the relationship between reproduction and genetic change. As Azevedo noted, understanding how mutation rates evolve may illuminate processes ranging from cancer and drug resistance to the broader capacity of living organisms to survive environmental change.

Subject of Research: The evolution of DNA mutation rates across organisms with sexual, asexual and self-pollinating reproductive modes.

Article Title: How Reproductive Strategies Shape the Speed of DNA Mutation

Web References: https://www.nsf.gov/awardsearch/show-award/?AWD_ID=2535706

Image Credits: University of Houston

Keywords: mutation rates, evolutionary biology, evolutionary genetics, genetic material, sexual reproduction, asexual reproduction, self-pollination, Tetrahymena, snails, mustard plants, genome stability, cancer evolution, antibiotic resistance, drug resistance, adaptive evolution, reproductive biology, microbial evolution

Blue mussels, Mytilus edulis, are far more than passive shellfish attached to rocks, piers and seabeds. A large individual can process as much as 100 litres of seawater per day, while dense mussel beds may contain millions of animals. Through filtration, they remove microscopic algae and suspended organic material from the water column, helping shape water clarity, nutrient cycling and the movement of energy through coastal ecosystems. Their shells also create a complex three-dimensional habitat, providing spaces where small crustaceans, worms, fish and plants can live. If many mussels reduce filtration at the same time, the consequences could extend beyond the animals themselves.

The study, published in the Journal of Helminthology, examined whether blue mussels could alter their behaviour when exposed to larvae from three species of parasitic flatworm. Two of the parasites are capable of infecting blue mussels, while the third normally infects fish and represents a lower or different threat to the mussels. The strongest behavioural response occurred in the presence of Himasthla elongata, a parasite whose larvae can penetrate and develop within mussel tissues. Exposed mussels reduced their filtration activity by 34 per cent compared with control animals. When H. elongata was combined with another mussel parasite, Renicola roscovita, filtration fell by 51 per cent.

The researchers also identified a direct relationship between the mussels’ feeding behaviour and parasite infection. Animals that continued filtering water at higher rates subsequently contained more parasites. This suggests that filtration is not merely a general physiological activity but also represents an important route of exposure. A mussel draws water across its gills, where food particles are captured and transferred into the digestive system. Parasite larvae present in the surrounding water can be swept into the same filtering system. By slowing the flow of water, the mussel may reduce the probability that infectious larvae will enter its body.

“This response is particularly interesting because the mussel changes its behaviour before the parasite has caused harm,” says PhD researcher Pernille Kibak, one of the study’s authors. The finding illustrates what ecologists call the “ecology of fear,” a concept first developed through studies of predators and prey. Animals often respond not only to direct attacks but also to the possibility of danger. A prey species may move away from a risky habitat, spend less time feeding or increase its vigilance even when no predator is visible. Similar mechanisms are now being identified in host-parasite relationships, where the costs of infection can include reduced growth, impaired reproduction and lower survival.

The experiments did not provide definitive evidence that blue mussels can identify individual parasite species with precision. The animals reacted differently to the three flatworms, but the responses varied substantially between individual mussels. This variation prevented the researchers from concluding that the mussels can reliably distinguish parasites that infect them from those that do not. Instead, the mussels may be responding to a broader chemical signature associated with biological danger. Their sensory systems can detect dissolved compounds in seawater, including chemical traces released by food, predators, injured members of their own species and potentially infected organisms.

A second series of experiments revealed that mussels reacted strongly even when the parasites themselves were absent. The researchers exposed the animals to seawater containing chemical cues from common periwinkles, small marine snails that do not directly harm blue mussels. However, periwinkles are important hosts in the life cycles of several parasitic flatworms. Parasite larvae can develop and reproduce inside the snails before being released into the water and moving on to later hosts, including mussels. Water containing only periwinkle cues caused mussel filtration to decline by almost 42 per cent compared with control conditions. The snails may therefore function as an indirect warning signal that parasite larvae are likely to be present.

The exact chemical compounds responsible for the reaction remain unknown. Water containing cues from parasites and infected snails did not reduce filtration significantly more than water containing cues from the snails alone. This result suggests that the periwinkle signal may be especially important, although it does not establish how the mussels detect it or whether the cue is produced by the snails, their associated microorganisms or the parasites living inside them. Because blue mussels are fixed in place by strong byssal threads, they cannot escape a dangerous area in the way a mobile animal can. Their main defence may instead be to interpret information carried by the water and temporarily reduce contact with it.

The protective value of this behaviour creates an ecological paradox. A mussel that filters less water may lower its chance of becoming infected, but it also takes in less food and contributes less to the removal of particles from the surrounding sea. Across a large mussel bed, widespread reductions in filtration could influence the deposition of organic material on the seabed, nutrient availability and the transfer of energy between the water column and bottom habitats. The researchers stress, however, that laboratory results cannot be transferred directly to natural ecosystems. Wild mussels experience fluctuating food concentrations, currents, temperatures and parasite densities, and they may compensate for short periods of reduced filtration by increasing activity later.

Climate change could make the question more urgent. Parasites pass through several life stages, and the development, survival and distribution of those stages are strongly influenced by temperature. Warmer seas may allow some parasites to expand into regions where they are currently rare or absent. Temperature also affects mussel metabolism, filtration and immune function, meaning that host and parasite responses may change simultaneously. The Aarhus University team is now studying mussels from colder areas with little or no current exposure to these parasites. If warming enables parasites to establish in those regions, the mussels may encounter a novel threat. Whether their behaviour will differ because they lack previous exposure could help scientists understand how parasite range shifts may reshape mussel ecology and coastal ecosystems.

Subject of Research: Blue mussel behavioural and filtration responses to parasitic flatworms and chemical cues from periwinkles.

Article Title: Avoidance of parasites by blue mussels Mytilus edulis: effect of parasite species and chemosensory cues

Web References: https://doi.org/10.1017/S0022149X26101643

References: Journal of Helminthology; DOI: 10.1017/S0022149X26101643

Image Credits: Karolin Janina Demtröder

Keywords: blue mussels, Mytilus edulis, parasites, ecology of fear, filtration, chemosensory cues, periwinkles, marine ecosystems, climate change, Aarhus University

The new delivery vehicle, known as FL0445-LNP, belongs to a class of microscopic particles that function somewhat like molecular containers. Lipid nanoparticles are assembled from fat-like molecules that form a protective structure around nucleic acids. Their outer surfaces are compatible with the watery environment of the body, while their lipid composition helps them interact with cell membranes. After being taken up by cells, the particles are designed to break down and release their cargo. This process allows the delivered mRNA or circular RNA to reach the cellular machinery responsible for translating genetic instructions into proteins.

The need for such protection arises from the inherent instability of linear mRNA. A conventional messenger RNA molecule has defined ends, including a cap structure that helps ribosomes recognize it and a tail that contributes to stability and translation. These same terminal regions, however, can also become targets for cellular enzymes that degrade RNA. Once the molecule is destroyed, protein production stops. This limited lifetime is useful for some applications, including transient vaccination, but it can be a disadvantage when a therapeutic protein needs to be produced over a longer period.

Circular RNA, or cirRNA, offers a different molecular architecture. Instead of having two exposed ends, the RNA strand is joined into a continuous loop. This configuration removes the terminal points that many degradation enzymes attack, potentially allowing the molecule to remain active in cells for longer periods. Because circular RNA lacks a natural stop point, ribosomes may repeatedly move around the loop and generate multiple copies of the encoded protein. Yet the structure also introduces a challenge: circular RNA does not naturally possess the cap-and-tail arrangement that makes linear mRNA highly efficient at initiating translation.

To address this limitation, Hiroshi Abe, Seigo Kimura, and colleagues at Nagoya University’s Integrated Research Consortium on Chemical Sciences and Department of Chemistry developed a capped circular RNA construct called Cap-cirRNA. The design retains the closed-loop structure associated with increased resistance to degradation while adding a cap-related feature intended to improve the initiation of protein synthesis. The researchers describe the approach as an effort to combine the durability of circular RNA with the strong translation performance of conventional mRNA. In principle, this could allow cells to produce a therapeutic protein efficiently without requiring repeated administration of unstable RNA molecules.

The team paired Cap-cirRNA with FL0445-LNP, a nanoparticle obtained from researchers at the Bioscience & Engineering Laboratories of FUJIFILM Corporation. A notable feature of the particle is the branched biodegradable chains within its ionizable lipid component. Conventional lipid nanoparticles often rely on lipids with more linear structures. By introducing branching, the researchers sought to create a more flexible internal environment capable of accommodating nucleic acids with different sizes, weights, and molecular shapes. That flexibility may be particularly important for circular RNA, whose geometry and physical properties differ from those of linear mRNA.

In comparative experiments, FL0445-LNP increased mRNA activity by approximately tenfold relative to conventional lipid nanoparticle formulations, while producing a negligible inflammatory response under the reported conditions. The finding is significant because inflammation remains an important consideration in RNA medicine. Lipid nanoparticles must be sufficiently active to deliver their cargo, but excessive immune stimulation can limit dosing, reduce tolerability, or complicate repeated treatment. A biodegradable and adaptable particle that combines efficient delivery with a restrained inflammatory profile could therefore be useful across several classes of nucleic-acid therapies.

For an initial therapeutic test, the researchers selected GLP-1, a peptide hormone that helps regulate blood glucose and appetite. Current GLP-1 medicines, including drugs used in obesity treatment, generally deliver the peptide or a peptide analogue directly through injection. An RNA-based strategy takes a different route: rather than supplying the finished protein, it provides cells with the genetic instructions needed to manufacture it. If those instructions remain active for an extended period, the approach could potentially reduce the frequency of injections. In the mouse experiments, FL0445-LNP successfully delivered both linear mRNA and Cap-cirRNA encoding GLP-1 and produced measurable biological activity.

Cap-cirRNA showed greater functional activity than the corresponding linear mRNA in the animal studies, although the researchers emphasize that the system requires further optimization before its therapeutic potential can be assessed in humans. Important questions remain concerning dose, tissue distribution, duration of protein production, immune responses after repeated administration, and the control of circular RNA activity. The amount of protein produced must also be carefully regulated, since prolonged or excessive expression could create safety risks depending on the therapeutic target. Nevertheless, the results provide evidence that a branched ionizable lipid nanoparticle can serve as a common delivery platform for chemically and structurally distinct RNA cargos.

The researchers envision applications extending beyond GLP-1 therapy. The platform could support next-generation vaccines in which durable protein production improves immune training, as well as cancer vaccines designed to present tumor-associated antigens to the immune system. It may also be relevant to genome-editing technologies, which require the temporary delivery of messenger RNA and editing components into cells. In genetic disorders caused by missing or defective proteins, the same strategy might provide instructions for producing a functional replacement protein. By pairing a versatile nanoparticle with RNA molecules engineered for either rapid or prolonged activity, the work points toward a broader toolkit for protein replacement, vaccination, and other forms of precision medicine.

Subject of Research: Cells

Article Title: A Branched Ionizable Lipid Nanoparticle Platform for Versatile In Vivo Delivery of Nucleic Acids: Validation from mRNA to Capped Circular RNA

News Publication Date: 19-Aug-2026

Web References: Nagoya University Integrated Research Consortium on Chemical Sciences: https://irccs.nagoya-u.ac.jp/ ; Nagoya University Department of Chemistry: https://www.chem.nagoya-u.ac.jp/en/

References: Cell Biomaterials, “A Branched Ionizable Lipid Nanoparticle Platform for Versatile In Vivo Delivery of Nucleic Acids: Validation from mRNA to Capped Circular RNA,” published 19-Aug-2026.

Image Credits: Sumeet Kulkarni, Nagoya University

Keywords: mRNA, circular RNA, Cap-cirRNA, lipid nanoparticles, FL0445-LNP, nucleic-acid delivery, GLP-1, RNA therapeutics, obesity treatment, cancer vaccines, genome editing, Nagoya University

Necroptosis and ferroptosis are distinct biological programs, but both can culminate in catastrophic loss of plasma-membrane integrity and the release of inflammatory intracellular contents. Necroptosis is a kinase-driven form of regulated necrosis that is typically associated with the receptor-interacting protein kinase 1, receptor-interacting protein kinase 3, and mixed lineage kinase domain-like pseudokinase axis. In response to signals such as tumor necrosis factor, pathogen-associated stress, damage-associated molecular patterns, or certain chemical insults, RIPK1 and RIPK3 can assemble into a signaling platform known as the necrosome. This promotes phosphorylation and oligomerization of MLKL, which then moves to the plasma membrane and disrupts its architecture. The resulting cellular rupture can release damage-associated molecular patterns and amplify local inflammation.

Ferroptosis follows a different molecular route. It is driven by iron-dependent oxidative damage to membrane lipids, particularly phospholipids containing polyunsaturated fatty acids. When intracellular iron availability and reactive oxygen species increase, susceptible lipids can undergo a chain reaction of peroxidation. Under normal conditions, antioxidant systems limit this process. Glutathione peroxidase 4 is one of the principal defenses because it reduces toxic lipid hydroperoxides to less-reactive lipid alcohols. Ferroptosis suppressor protein 1 provides another protective mechanism by supporting the regeneration of reduced coenzyme Q10, a radical-trapping antioxidant. When these systems are overwhelmed or disabled, lipid peroxide accumulation destabilizes membranes and can ultimately produce irreversible cell damage.

Although the initiating signals differ, the two pathways can be influenced by overlapping cellular conditions. Redox imbalance, mitochondrial dysfunction, altered lipid metabolism, iron handling, and inflammatory signaling may affect both necroptotic and ferroptotic sensitivity. In some disease settings, suppression of one form of regulated death may also shift cellular stress toward another. This possibility is particularly important in acute and chronic organ injuries, where damaged tissues may contain multiple cell populations exposed to cytokines, hypoxia, metabolic disruption, and oxidative stress at the same time. According to the review, these interconnections create a rationale for investigating compounds that can modulate more than one regulated-death mechanism.

The NecroFerrin concept is based on combining two pharmacological activities within a single molecular framework. One activity would interfere with necroptotic signaling, potentially by inhibiting RIPK1-dependent events. The second would limit the propagation of lipid radicals and thereby reduce ferroptotic membrane damage. The review highlights RIPROStatins as an example of this strategy. These compounds are described as combining RIPK1 inhibition with radical-trapping antioxidant properties, bringing together suppression of a protein-kinase-controlled pathway and chemical interception of the lipid oxidation reactions that drive ferroptosis. Such a design is intended to address both upstream signaling and downstream membrane injury.

The proposed mechanism also involves molecular systems that connect protein quality control with oxidative cell death. The review discusses heat shock protein 90 as one example of a cellular chaperone that can influence these pathways. HSP90 helps stabilize and regulate numerous proteins, and it may participate in chaperone-mediated autophagic degradation of GPX4 under certain conditions. Because GPX4 is central to the removal of lipid peroxides, changes in its abundance or activity can strongly affect ferroptotic vulnerability. This relationship illustrates why a compound’s effects may extend beyond a single signaling protein: cellular chaperones, autophagy, antioxidant capacity, iron metabolism, and membrane composition can collectively determine whether a stressed cell survives or crosses the threshold into regulated necrosis.

The review places NecroFerrins within the broader field of polypharmacology, which seeks to use one compound to influence several biologically connected targets. In complex diseases, single-target drugs may be limited by pathway redundancy, compensatory signaling, or the simultaneous activation of multiple injury programs. A molecule that blocks RIPK1-dependent necroptosis while also neutralizing lipid radicals could, in principle, provide broader protection than either a selective necroptosis inhibitor or a ferroptosis inhibitor alone. However, the authors emphasize that dual activity does not automatically translate into therapeutic success. The balance between potency, selectivity, tissue distribution, metabolic stability, and toxicity will determine whether such molecules can be developed into useful treatments.

This caution is especially relevant because necroptosis and ferroptosis are not exclusively harmful processes in every biological context. Regulated cell death contributes to host defense, tissue remodeling, elimination of damaged cells, and responses to infection. Broadly suppressing these mechanisms could therefore interfere with beneficial immune or homeostatic functions. In addition, the same compound may behave differently across organs because cells vary in their expression of RIPK1, RIPK3, MLKL, GPX4, FSP1, antioxidant enzymes, iron-storage proteins, and lipid-processing pathways. Rigorous studies will be required to establish whether a candidate NecroFerrin acts through the intended mechanisms in living tissues and whether it can protect organs without producing undesirable immunological or metabolic effects.

The authors present the dual-inhibition concept as a framework for future chemical biology rather than as a completed therapeutic solution. Experimental validation will need to distinguish direct pathway inhibition from nonspecific antioxidant or cytoprotective effects. Researchers will also need to determine how these molecules perform in disease models involving ischemia-reperfusion injury, inflammation, infection, neurodegeneration, or organ fibrosis, where regulated cell-death pathways may operate simultaneously. Biomarkers of necroptosis, ferroptosis, lipid peroxidation, iron status, and inflammatory damage could help identify patients or disease stages most likely to benefit. By viewing regulated cell death as an interconnected network, the review argues that future drug discovery may move beyond the question of how to inhibit one pathway and instead ask whether several converging mechanisms can be controlled with a carefully designed single molecule.

Subject of Research: Cells

Article Title: NecroFerrins as dual therapeutic inhibitors targeting necroptosis and ferroptosis

Web References: https://doi.org/10.70401/fos.2026.0041 ; https://smart.servier.com/ ; https://creativecommons.org/licenses/by/4.0/

References: Delehouzé, Claire, and Stéphane Bach. “NecroFerrins as dual therapeutic inhibitors targeting necroptosis and ferroptosis.” Ferroptosis and Oxidative Stress. DOI: 10.70401/fos.2026.0041.

Image Credits: Claire Delehouzé and Stéphane Bach, 2027; adapted from Servier Medical Art, licensed under CC BY 4.0.

Keywords: Necroptosis, ferroptosis, NecroFerrins, RIPK1, RIPK3, MLKL, lipid peroxidation, GPX4, FSP1, oxidative stress, regulated cell death, polypharmacology, RIPROStatins

The study, published in Nature Plants, examined the biogeographical distributions of 15 taxonomic traits. These traits describe fundamental aspects of plant biology, including whether a species is woody or herbaceous, evergreen or deciduous, fleshy-fruited or dry-fruited, annual or perennial, and whether its flowers are bisexual, zygomorphic or sympetalous. By comparing the relative representation of these traits across regions, the researchers looked for coordinated changes in plant composition rather than asking where any single characteristic was most common. The result was a statistical map of global angiosperm diversity in which most regional differences can be summarized through a limited number of major dimensions.

The first and strongest dimension describes a broad hydrothermal gradient. At one end are warm, wet regions characterized by a greater prevalence of woody, evergreen and fleshy-fruited plants. These areas include environments where year-round or seasonally reliable moisture can support long-lived vegetation and investment in persistent stems and leaves. Fleshy fruits, often dispersed by animals, are also prominent in many humid ecosystems. At the opposite end of the dimension, cooler or drier regions contain higher proportions of herbaceous species and plants producing dry fruits. These plants may complete their life cycles more rapidly, tolerate seasonal stress, or rely on wind and mechanical dispersal rather than animal-mediated fruit consumption.

This first axis does not represent a simple division between tropical and temperate floras. Instead, it integrates temperature and water availability into a biological gradient that cuts across multiple continents and vegetation types. Hydrothermal conditions influence plant metabolism, growing-season length, tissue construction and reproductive timing, so it is not surprising that several traits respond in parallel. What is striking is the consistency of those relationships at the global scale. A region’s climate appears to help determine not only which species can survive there, but also the overall balance of structural and reproductive strategies represented in its angiosperm flora.

A second dimension captures a different combination of traits. It is associated with a higher prevalence of zygomorphic flowers, sympetalous flowers, bisexual flowers and annual life cycles, particularly in environments that are warm but arid. Zygomorphic flowers have bilateral symmetry, while sympetalous flowers possess petals fused into a tube or other connected structure. Both features can influence pollinator interactions, potentially guiding visitors toward particular floral rewards or placing pollen in precise locations on their bodies. Annual plants, meanwhile, can exploit brief windows of favorable conditions by germinating, flowering and setting seed before drought becomes severe.

The second dimension therefore points toward a distinctive hot-arid floral and life-history profile rather than merely extending the wet-to-dry gradient represented by the first axis. In seasonally harsh landscapes, rapid reproduction may be advantageous, while specialized floral architecture can reflect the ecological and evolutionary dynamics of pollination in open environments. The finding does not mean that every desert or semi-desert plant shares the same traits, nor that climate alone determines floral form. Instead, it shows that these characteristics are more likely to occur together regionally than would be expected if each trait varied independently.

The researchers also investigated how much trait diversity exists within individual regions. Within-region trait divergence was greatest near the median of the first dimension, suggesting that areas occupying an intermediate position along the major hydrothermal gradient can contain especially contrasting plant strategies. Such regions may combine species associated with different climatic conditions, habitats or historical floristic sources. Divergence also increased along the second dimension, indicating that regions characterized by the hot-arid floral syndrome may contain substantial internal separation among trait combinations. This pattern adds an important layer to the global map: regions can be similar in their average trait composition while still harboring species with markedly different ecological strategies.

Environmental variables explained part of the coordinated distribution of traits, but the role of regional phylogenetic structure became increasingly important from the first dimension to the second. Phylogenetic structure measures whether the species found in a region are more closely related, or more distantly related, than expected under a specified null model. Strong clustering can indicate that particular evolutionary lineages have been filtered into an environment, while overdispersion may suggest the independent arrival of similar traits from multiple branches of the angiosperm tree. The study’s results imply that climate is especially influential in shaping the broadest trait gradient, whereas evolutionary history contributes more strongly to the finer structure associated with the second dimension.

This relationship is particularly evident in arid regions, where phylogenetic clustering is consistent with the preferential representation of lineages carrying suites of traits suited to water limitation. Drought tolerance is rarely controlled by a single characteristic. It can involve coordinated changes in plant architecture, tissue longevity, reproductive timing, fruiting strategy and floral biology. When related lineages share several such adaptations, dry environments may repeatedly favor entire branches of the evolutionary tree rather than isolated species. That process can make regional floras appear evolutionarily clustered while also producing recognizable trait combinations across distant parts of the world.

The researchers describe their findings as a step beyond cataloguing individual biogeographical patterns. Previous studies have often focused on one trait at a time, such as leaf habit, fruit type or floral symmetry. The new analysis instead asks how traits covary across regions and whether those relationships are repeatable worldwide. Its low-dimensional structure offers a framework for comparing floras that may be separated by oceans but shaped by similar environmental pressures or evolutionary filters. As climate change alters temperature regimes, precipitation patterns and the duration of favorable growing seasons, this framework could help scientists anticipate not only which species may move or decline, but how the overall composition of plant communities may reorganize. The global flowering-plant map, the study suggests, is not an unstructured mosaic: it is governed by a small set of powerful interactions among climate, ecological strategy and the history of life.

Subject of Research: Global biogeographical variation and covariation of angiosperm taxonomic traits across more than 320,000 species.

Article Title: Biogeographical variation of angiosperm taxonomic traits exhibits a globally consistent structure

Article References: Zhang, C., Zhang, Q., Sun, X. et al. Biogeographical variation of angiosperm taxonomic traits exhibits a globally consistent structure. Nat. Plants (2026). https://doi.org/10.1038/s41477-026-02358-w

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41477-026-02358-w

Keywords: angiosperms, plant biogeography, plant traits, biodiversity, climate gradients, hydrothermal gradients, phylogenetic structure, floral traits, arid ecosystems, global ecology

The study, published in PRX Life, focuses on biopolymer condensates, liquid-like droplets formed when proteins, nucleic acids, or combinations of both gather into concentrated compartments. Unlike membrane-bound organelles, these condensates are assembled through physical processes such as liquid-liquid phase separation. Their interiors can concentrate specific molecules, creating temporary reaction environments that help regulate gene expression, signaling, stress responses, and other essential cellular functions. Because condensates can form, merge, dissolve, and change their internal organization rapidly, their material properties are closely connected to their biological roles.

The droplets are not simply passive blobs of liquid. Their viscosity, stiffness, surface tension, internal molecular arrangement, and ability to flow can determine how they interact with other cellular components. A condensate that becomes unusually viscous or rigid may fail to merge correctly, trap molecules that should remain mobile, or persist longer than it should. Such changes have been associated with abnormal cellular states and are of particular interest in research on neurodegenerative diseases, where proteins and nucleic acids can form persistent, dysfunctional assemblies. Yet measuring these properties directly is difficult because the droplets are microscopic, soft, and easily altered by physical contact.

Conventional measurement techniques can introduce precisely the disturbances scientists are trying to avoid. Touching a droplet with a probe may deform it, move molecules within it, or change its shape and composition. Even the process of placing a droplet on a surface can modify its behavior. To overcome this problem, the Osaka-led team developed an acoustic tweezer system that uses ultrasound to exert forces on condensates without a mechanical tool ever contacting them. The device creates a controlled acoustic field, allowing droplets to be captured at a specific location, held in place, and arranged for observation.

“ We fabricated a device that creates an acoustic force that can trap condensates at a specific point,” explains lead author Kichitaro Nakajima. In practical terms, the system uses the pressure distribution generated by sound waves to influence the motion of the droplets in solution. When the acoustic forces are balanced appropriately, a condensate can be confined near a defined position. This form of acoustic manipulation is related to the broader field of acoustic tweezers, in which sound is used to control small objects ranging from cells to particles without the need for physical contact.

To test the approach, the researchers studied condensates made from polyadenylic acid, a nucleic-acid-based polymer. These condensates are particularly useful for a proof-of-concept experiment because their properties respond sensitively to salt concentration. Changing the concentration of dissolved salt can alter the interactions among polymer molecules, affecting how the droplets form and how they behave mechanically. The researchers therefore expected that changes in the chemical environment would produce measurable changes in droplet behavior under acoustic trapping.

The experiments showed that the condensates could be efficiently trapped and aligned using the acoustic force. This allowed the team to observe the droplets while minimizing direct disturbance. The system also made it possible to bring two condensates together and examine what happened as they merged. Droplet fusion is an important physical process: in a simple liquid system, two droplets may rapidly combine into one larger sphere, but the speed and manner of fusion can reveal information about viscosity, interfacial tension, and molecular organization. Watching this process under controlled conditions gave the researchers another way to examine the mechanics of the condensates.

The team’s analysis went beyond simply holding the droplets still. When a condensate is trapped by sound, its natural movement in the surrounding solution changes. That movement includes fluctuations caused by thermal energy and interactions between the droplet and its fluid environment. By analyzing how the droplet moved under the acoustic force, the researchers extracted information about its stiffness and the condition of the molecules inside it. They then developed a framework for estimating droplet stiffness from the observed response of the trapped condensate.

This approach effectively turns microscopic motion into a mechanical measurement. A softer droplet may respond differently to the acoustic field than a stiffer one, while changes in internal molecular interactions can influence both its movement and its response during fusion. The method therefore provides a way to connect visible behavior with properties that are otherwise difficult to measure directly. Importantly, the technique does not require the droplet to be attached to a surface or compressed by a probe, preserving a more natural solution-based environment.

The researchers believe acoustic tweezers could become a broadly useful tool for investigating soft biological materials. By enabling contactless measurements of condensate mechanics, the technology may help scientists understand how these droplets function in healthy cells and how their physical properties change during disease. It could also support studies of other delicate materials whose behavior is easily disrupted by conventional instruments. Although the current work is a proof of concept using polyadenylic-acid condensates, the underlying strategy offers a promising route toward mapping how molecular composition, chemical conditions, and mechanical properties interact inside biomolecular droplets. In the long term, such information could contribute to a clearer understanding of condensate-related dysfunction and guide the search for therapies targeting diseases in which these dynamic cellular compartments go awry.

Subject of Research: Not applicable

Article Title: Mechanical profiling of biopolymer condensates through acoustic trapping

News Publication Date: 17-Aug-2026

Web References: https://doi.org/10.1103/kl9v-5ywv

References: PRX Life, “Mechanical profiling of biopolymer condensates through acoustic trapping,” DOI: 10.1103/kl9v-5ywv

Image Credits: K. Nakajima et al., PRX Life (American Physical Society)

Keywords: Acoustic tweezers, biopolymer condensates, biomolecular droplets, biophysics, acoustic trapping, soft matter physics, cell biology, neurodegenerative diseases, microfluidic droplets, Brownian motion, applied acoustics, natural polymers

The investigation followed 21 adults before and after seasonal influenza vaccination. The researchers grouped participants according to their baseline levels of antibodies directed against hemagglutinin, or HA, the major surface glycoprotein used by influenza viruses to attach to and enter host cells. HA-specific antibody titers provide an indication of existing humoral immunity, but they do not fully describe the cellular processes that generate or refine antibody responses. To examine those processes, the team combined flow cytometry with B-cell receptor sequencing and monoclonal antibody characterization. This integrated approach enabled the scientists to track changes in HA-binding B-cell populations, analyze immunoglobulin gene sequences, and test the binding and neutralizing properties of antibodies produced by individual B-cell lineages.

The researchers identified clear differences in the HA-binding B-cell responses of people with different pre-vaccination antibody levels. Participants with higher baseline titers showed increased frequencies of HA-positive B cells carrying a naive-like phenotype, defined by expression of CD27 and IgD markers consistent with less antigen-experienced cells. Naive B cells have not undergone the extensive selection and refinement typically associated with mature memory responses. Their greater representation after vaccination suggests that individuals with substantial pre-existing antibody may recruit or maintain B-cell populations that have experienced less maturation, rather than exclusively reactivating highly evolved memory lineages generated by earlier influenza exposures.

B-cell receptor sequencing provided additional evidence that the antibody response differed according to baseline immunity. B-cell receptors, which are membrane-bound forms of antibodies, carry genetic signatures of a cell’s developmental history. During an immune response, activated B cells can undergo somatic hypermutation, a process that introduces mutations into antibody variable-region genes. Cells whose receptors acquire advantageous mutations may be preferentially selected and expanded, improving their ability to recognize antigen. The study found that B-cell receptors associated with participants in the lower-titer groups displayed greater levels of mutation than those observed in the higher-titer groups. This pattern is consistent with a response involving more extensively matured antibody lineages.

The lower-titer groups also showed broader class switching. B cells initially produce antibodies such as immunoglobulin M before switching to other antibody classes, including immunoglobulin G, which can have different tissue distributions and functional properties. Class-switch recombination changes the constant region of the antibody without altering the antigen-binding sequence, allowing an immune response to acquire new biological functions while retaining target recognition. More extensive class switching, together with higher mutation levels, indicated that B-cell lineages in the lower-baseline-antibody participants had undergone a greater degree of evolutionary refinement. The researchers’ analysis therefore linked reduced pre-existing HA antibody levels with a response that appeared more mature at the molecular level.

The functional properties of antibodies generated by these lineages reinforced the sequencing results. Monoclonal antibodies from the lower-titer groups demonstrated broader neutralizing activity against historical influenza strains, suggesting that they recognized conserved features shared across viruses from different periods. Neutralization is a particularly important measure because antibody binding alone does not necessarily prevent infection. Antibodies that block viral attachment, interfere with membrane fusion, or otherwise inhibit productive replication can provide more meaningful protection. The broader activity observed in the lower-titer group indicates that the associated B-cell lineages were not simply producing more antibodies, but were generating antibodies with a wider capacity to counter antigenically diverse influenza viruses.

By contrast, the response associated with higher pre-vaccination antibody levels appeared to contain a larger contribution from less-mature B-cell populations. One possible explanation is that abundant circulating antibodies may alter the amount, form, or persistence of vaccine antigen available to stimulate B cells. Pre-existing antibodies can bind antigen and influence its transport, uptake, and presentation, potentially changing which B-cell clones receive activation signals. They may also create selective conditions in which some previously generated lineages are inhibited while other, less-experienced populations are recruited. The present study establishes an association rather than proving a single mechanism, but its results support the idea that baseline antibody concentrations can shape the cellular pathway followed after vaccination.

The findings also illustrate why vaccine responses cannot be evaluated solely by measuring the overall concentration of antibodies in blood. Two individuals may reach similar post-vaccination antibody levels while producing antibodies with different degrees of mutation, class switching, lineage diversity, or cross-strain activity. By examining B-cell phenotypes, receptor sequences, and monoclonal antibody function together, the researchers were able to distinguish these qualitative features. Such information may be particularly valuable for influenza, where antigenic drift continually changes the HA proteins targeted by immunity. A response focused on strain-specific sites may lose effectiveness as the virus evolves, whereas antibodies recognizing conserved regions could retain activity across multiple seasons.

The study adds to growing evidence that immune history is an important determinant of vaccine performance. Previous infections and vaccinations are not simply cumulative sources of protection; they can redirect the composition and evolution of later B-cell responses. The researchers emphasize that different pre-existing antibody levels were associated with different patterns of maturation and antibody breadth following influenza vaccination. Further studies involving larger and more diverse populations will be needed to determine whether the same relationships occur across age groups, vaccine formulations, influenza subtypes, and repeated vaccination histories. Nonetheless, the work provides a framework for investigating how baseline immunity influences vaccine-induced B-cell evolution and may support the development of influenza vaccines designed to promote broadly neutralizing antibodies despite substantial variation in individual immune backgrounds.

Subject of Research: Cells

Article Title: Pre-existing hemagglutinin-specific antibody levels are associated with B-cell repertoire maturation and antibody breadth after influenza vaccination

Web References: https://doi.org/10.1016/j.virs.2026.08.007

References: Wang W, Sun Y, Liu Q, Xia Y, Wang J, Hu M, Kong M, He J, Gao R, Gao Y. “Pre-existing hemagglutinin-specific antibody levels are associated with B-cell repertoire maturation and antibody breadth after influenza vaccination.” Virologica Sinica. DOI: 10.1016/j.virs.2026.08.007

Image Credits: Wei Wang, Yan Sun, Qing Liu, Yidan Xia, Jing Wang, Minhao Hu, Mengyao Kong, Jun He, Rongbao Gao, Yong Gao

Keywords: influenza vaccination, hemagglutinin, B cells, B-cell receptor sequencing, antibody maturation, antibody breadth, neutralizing antibodies, pre-existing immunity, influenza viruses, vaccine response

For decades, coronin proteins have occupied a familiar place in cell biology textbooks. They have generally been described as regulators of actin, the filament-forming protein that builds much of the cytoskeleton and helps cells maintain their shape, move through tissues, organize their internal components and respond to changes in their environment. A new study from the University of Basel now challenges that widely accepted interpretation. Researchers led by Professor Jean Pieters at the Biozentrum report that coronins are largely dispensable for the overall organization of the actin cytoskeleton in the cellular systems they examined. Instead, their findings point toward a broader and potentially more important role for these proteins in intracellular signaling, while also raising concerns about experimental methods that may have reinforced the conventional view.

Coronins are an evolutionarily conserved family of proteins found across the animal kingdom, including in single-celled organisms and humans. Their biological importance is not in question: previous research has connected coronins to immune responses, development, cell survival and the maintenance of normal immune-cell populations. The controversy concerns how these proteins perform those functions. Because coronins have repeatedly been observed near actin filaments, and because some experimental systems have suggested that they bind or influence actin, the family has commonly been classified as a group of actin effectors. In molecular terms, an actin effector would be expected to directly associate with actin filaments or with the machinery that controls their assembly, disassembly, branching or movement. The Basel team’s reassessment suggests that this framework may have overstated the centrality of coronins to cytoskeletal control.

The researchers approached the question by examining native coronin proteins through a broad range of experimental strategies. Their work was motivated in part by years of observations in which the laboratory failed to find consistent evidence that coronins directly bind actin or modulate actin behavior across multiple model systems. One of the strongest arguments against an essential global role for coronins came from cells lacking these proteins. According to the study, such cells were still able to organize and remodel their actin networks in a manner that was broadly comparable to cells containing coronins. They could preserve the filamentous structures required for cellular architecture and dynamic rearrangement, indicating that coronins are not universally necessary for the basic construction or maintenance of the actin cytoskeleton.

That conclusion does not mean that coronins can never interact with actin, nor does it eliminate the possibility that they influence specific actin-dependent processes under particular conditions. Cellular regulation is rarely binary. A protein can have a detectable association with a cytoskeletal structure without being essential for the structure’s overall organization. It may also affect actin indirectly by changing signaling pathways, membrane trafficking, cellular metabolism or the activity of other regulatory proteins. The Basel researchers therefore describe their results as a reassessment rather than an absolute rejection of every proposed connection between coronins and actin. Their central claim is that the evidence does not support treating coronins primarily as universal actin regulators, especially when broader cellular functions are taken into account.

A particularly striking finding concerns the molecular tags commonly used to study proteins inside living cells. Scientists frequently attach fluorescent or other biochemical labels to a protein of interest so that they can follow its location, movement and interactions using microscopy or biochemical assays. These tags are often regarded as functionally neutral, but the researchers found that tagging coronin proteins can cause them to lose normal activity and can substantially alter where they accumulate within the cell. Such changes could have serious consequences for interpretation. A tagged coronin that no longer behaves like its native counterpart might appear to localize near actin, fail to participate in signaling or produce an artificial phenotype. Experiments based on that altered protein could then be cited as evidence for a biological role that does not occur in the same way under physiological conditions.

The study also highlights the problem of antibody specificity. Antibodies are widely used to detect proteins in techniques such as immunofluorescence microscopy, western blotting and immunoprecipitation. Their value depends on recognizing the intended target while avoiding unrelated proteins. The Basel team reports that several antibodies commonly used to detect coronins lacked sufficient specificity. In practice, this means that a signal attributed to a coronin may partly or entirely reflect binding to another protein. When combined with the effects of artificial molecular tags, nonspecific antibodies can create a chain of misleading observations: a protein may appear to occupy a particular cellular compartment, associate with actin or change in abundance even though the measured signal does not accurately represent the native molecule. The researchers say these concerns reinforce wider calls for greater antibody validation throughout biomedical research.

The alternative picture emerging from the study places coronins more prominently within cell-signaling networks. Signaling proteins act as molecular communication systems, transmitting information from receptors and environmental cues to the machinery that controls gene expression, survival, proliferation, movement and immune activity. In immune cells, coronins have previously been implicated in pathways that regulate the number and behavior of T cells. T cells are essential components of adaptive immunity, recognizing infected or abnormal cells and coordinating targeted defenses. Maintaining the correct number of these cells is crucial: too few can weaken protection against infection and cancer, while excessive or improperly controlled populations can contribute to harmful inflammation or autoimmunity. The researchers emphasize that coronin-dependent signaling is important for preserving normal T-cell numbers, suggesting that the family’s physiological impact may be better understood through its effects on communication pathways than through a primary role in actin filament organization.

This signaling-centered interpretation may also explain why coronins have repeatedly been connected to the cytoskeleton. Actin is not merely a structural scaffold; it is deeply integrated with signaling. Receptors, enzymes and signaling complexes can move along or assemble near actin-rich regions, while signals from the cell surface can rapidly reorganize actin filaments. A coronin could therefore influence cytoskeletal behavior indirectly by controlling a signaling pathway, or it could participate in a specialized local interaction without directing the entire actin network. Conversely, changes in actin organization could affect coronin-dependent signaling by altering the positioning or accessibility of molecular complexes. The relationship may thus be reciprocal and context-dependent rather than a simple model in which coronins directly regulate actin throughout the cell.

The implications extend beyond the coronin family. The study illustrates how scientific ideas can become entrenched when observations are repeated using tools that are treated as neutral but can alter the biology under investigation. It also demonstrates why conclusions about protein function are strongest when supported by native-protein experiments, genetic loss-of-function approaches, independent detection methods and careful controls for reagent specificity. By revisiting the assumptions surrounding coronins, the University of Basel researchers open new avenues for investigating how these proteins contribute to signal transduction, immune-cell maintenance, cellular survival and communication. The findings do not erase decades of work, but they suggest that future studies should distinguish more carefully between direct molecular activity, indirect regulation and experimental artefact. In doing so, they may help reveal why coronins have been conserved across evolution and how their signaling functions support the delicate balance of life inside cells.

Subject of Research: Coronin proteins, their proposed roles in actin cytoskeleton regulation, cellular signaling and immune-cell maintenance.

Article Title: Reassessment of the roles of coronin proteins as actin effectors and in signaling

Web References: https://doi.org/10.1371/journal.pbio.3003904

References: PLOS Biology article, “Reassessment of the roles of coronin proteins as actin effectors and in signaling,” DOI: 10.1371/journal.pbio.3003904

Image Credits: Biozentrum, University of Basel, Roko Gvozdenica Sipic

Keywords: coronin proteins, actin cytoskeleton, cell signaling, immune cells, T cells, protein tagging, antibody specificity, cellular biology, Biozentrum University of Basel, PLOS Biology

Church is widely recognized for contributions that have shaped several major branches of contemporary biomedicine. His career has included pioneering work in genome sequencing, genome editing, synthetic biology, gene therapy, cellular reprogramming, artificial intelligence-based protein engineering, and the study of aging. He has also been involved in landmark initiatives such as the Human Genome Project, the Personal Genome Project, the BRAIN Initiative, and Genome Project-write. Together, these efforts have helped transform DNA from a biological molecule studied primarily through observation into an increasingly programmable platform. Modern sequencing can now read genetic information at enormous scale, while editing technologies can alter selected sequences and synthetic biology can assemble new genetic systems for research or therapeutic use.

That convergence is particularly important to longevity research, where scientists are investigating the molecular mechanisms that cause tissues and organs to lose resilience over time. Aging is not controlled by a single gene or pathway. Instead, it involves interacting processes that include the accumulation of DNA damage, epigenetic changes that disrupt gene regulation, mitochondrial dysfunction, chronic inflammation, loss of protein quality control, cellular senescence, stem-cell exhaustion, and alterations in intercellular communication. These mechanisms can reinforce one another, gradually reducing an organism’s ability to repair damage and maintain stable physiological function. Church’s participation at ARDD 2026 is expected to focus attention on how emerging technologies might intervene in these systems, either by correcting damage, resetting cellular states, replacing dysfunctional cells, or improving the body’s capacity for repair.

One of the most closely watched possibilities is cellular reprogramming. In experimental systems, combinations of transcription factors can push mature cells toward a more developmentally flexible state, sometimes restoring molecular features associated with youth while preserving aspects of cellular identity. The challenge is to achieve rejuvenation without causing uncontrolled proliferation or loss of tissue function. Gene therapy offers another route, using engineered viral vectors or other delivery systems to introduce, silence, or regulate genetic instructions inside selected cells. Such approaches could potentially target age-related disorders, although delivery, immune reactions, durability, dosage, and safety remain major barriers. Advances in protein engineering and artificial intelligence may also accelerate the discovery of therapeutic molecules capable of modulating difficult biological targets.

Church joins ARDD at a moment when longevity science is moving from exploratory laboratory research toward increasingly organized drug-development programs. Pharmaceutical and biotechnology companies are investigating interventions designed to influence senescent cells, metabolic regulation, inflammation, DNA repair, mitochondrial performance, and other biological processes associated with aging. The field’s central ambition is not simply to extend lifespan, but to lengthen healthspan—the period during which people remain physically capable, cognitively functional, and free from disabling disease. Achieving that goal will require rigorous clinical trials capable of demonstrating meaningful improvements in health outcomes rather than relying only on changes in molecular biomarkers. Researchers must also determine whether an intervention that benefits one organ or pathway can produce durable advantages across the entire body.

The meeting will therefore examine a question that has moved increasingly into mainstream biomedical discussion: how close is science to a genuine longevity revolution? The answer depends on whether promising findings in cells and laboratory animals can be translated into safe, reproducible effects in humans. Biological aging differs across tissues and individuals, and the biomarkers used to measure it—including epigenetic patterns, inflammatory signals, protein profiles, and physiological performance—do not always provide the same picture. A treatment that makes one molecular clock appear younger may not necessarily reduce disease or improve survival. For that reason, the next stage of the field will depend on carefully designed studies, long-term monitoring, improved measurement technologies, and collaboration among basic scientists, clinical investigators, regulators, and commercial developers.

Vadim Gladyshev, Executive Chair of ARDD and Professor of Medicine at Harvard University, said that aging biology has become one of biomedical science’s most promising frontiers, while emphasizing the need to connect fundamental discoveries with interventions that improve healthspan. Morten Scheibye-Knudsen, Co-Chair of ARDD and Associate Professor at the University of Copenhagen, described the conference’s move to Boston as a new chapter for the event, placing it within one of the world’s strongest biomedical innovation ecosystems. He also pointed to the field’s increasing emphasis on translation, as discoveries in aging biology are increasingly being evaluated according to their potential to become medicines rather than remaining isolated laboratory findings.

ARDD 2026 will be anchored by Tier 1 sponsors Insilico Medicine and Eli Lilly, with the McKinsey Health Institute serving as Sole Knowledge Partner. Tier 3 sponsors include AbbVie, AniVC, AstraZeneca, BioAge Labs, Biocytogen, Cambrian Bio, Cyclarity Therapeutics, Dior, GlycanAge, Gordian Biotechnology, Human Longevity, the Institute for Healthier Living Abu Dhabi, LongeVC, Maxwell Biosciences, Nestlé, Tally Health, and TruDiagnostic. Synaro Capital, The Cat Health Company, and PranaGen Bioscience are supporting the meeting as Tier 4 sponsors, while Estée Lauder, Morgan Stanley, the Intrinsic Capacity Frailty & Sarcopenia Research Conference for Healthy Longevity, and QuadraScope are listed as Tier 5 sponsors. The breadth of participation reflects the growing financial and industrial interest in therapies that could address the biological drivers of age-related decline.

Alex Zhavoronkov, Co-Chair of ARDD and CEO of Insilico Medicine, said Church has repeatedly helped move ideas once regarded as speculative toward serious scientific and technological possibility. His presence captures the conference’s larger purpose: connecting ambitious biological concepts with the researchers, companies, and investors capable of testing and developing them. Now in its 13th year, the Aging Research & Drug Discovery Meeting describes itself as the world’s largest meeting dedicated to aging and longevity biotechnology. The 2026 gathering will also receive support from the Nordic Aging Society, a nonprofit scientific organization focused on aging research and collaboration across the Nordic region and beyond. Organizers are inviting media inquiries and interview requests through ardd@pharma.ai, while additional information is available at agingpharma.org.

Subject of Research: Aging research, longevity biotechnology, genomics, cellular reprogramming, gene therapy, and the development of therapies targeting age-related decline.

Article Title: George Church to Deliver Featured Address at ARDD 2026 on the Future of Longevity Science

News Publication Date: August 18, 2026

Web References: agingpharma.org

Image Credits: ARDD 2026

Keywords: George Church, ARDD 2026, aging research, longevity science, longevity biotechnology, genomics, gene therapy, cellular reprogramming, synthetic biology, healthspan, Harvard University, Insilico Medicine, drug discovery