One particularly pernicious category of DNA lesions is DNA–protein crosslinks (DPCs). These covalent linkages between DNA strands and associated proteins can be instigated by endogenous metabolites such as aldehydes, including formaldehyde, or exogenous exposures like chronic alcohol consumption. Moreover, they may arise as inadvertent errors during DNA replication or repair processes. DPCs pose a formidable impediment to DNA polymerases, causing replication fork stalling and hampering faithful chromosome segregation. The persistence of these crosslinks threatens the integrity of the genome and jeopardizes cellular viability.

A pivotal guardian against the DNA–protein crosslink menace is the metalloprotease enzyme SPRTN. This specialized protease recognizes and cleaves DPCs, facilitating their removal and thereby enabling the resumption of replication fork progression. Genetic mutations that impair SPRTN function underlie Ruijs-Aalfs syndrome, a rare hereditary disorder characterized by premature onset bone deformities and liver cancer in adolescence. Despite recognition of SPRTN’s role, the downstream pathological mechanisms stemming from its loss have remained elusive, obstructing therapeutic development.

Recent investigations spearheaded by Prof. Ivan Ðikić and colleagues at Goethe University Frankfurt have elucidated heretofore unappreciated systemic consequences of SPRTN deficiency. Employing both cultured cell models and genetically engineered murine systems, their research demonstrated that the absence of functional SPRTN exacerbates the accumulation of DNA damage within the nucleus. Strikingly, this unrepaired damaged DNA was observed to aberrantly translocate into the cytoplasm, breaching the nuclear envelope’s compartmentalization.

This cytoplasmic presence of nuclear DNA incites a potent innate immune response. Cells interpret cytosolic DNA as a pathogenic danger signal, typically indicative of viral or bacterial invasion or oncogenic transformations. Specifically, extraneous DNA in the cytoplasm activates the cyclic GMP-AMP synthase (cGAS) – stimulator of interferon genes (STING) signaling axis. This pathway triggers an inflammatory cascade, promoting secretion of cytokines and chemokines that recruit immune effectors, thus establishing a state of chronic inflammation.

The implications of this pathological immune activation were particularly pronounced in vivo. Mouse embryos deficient in SPRTN exhibited robust cGAS-STING activation, resulting in pervasive inflammation that persisted into adulthood. The sustained immune assault disproportionately affected vital organs such as the lungs and liver, culminating in premature mortality and phenotypes mimicking accelerated aging. Therapeutic blockade of this immune axis ameliorated many adverse manifestations, underscoring the causal role of inflammation driven by cytoplasmic DNA in the disease process.

These findings reveal that the pathogenic impact of unrepaired DNA-protein crosslinks transcends genomic instability alone, extending to profound systemic inflammatory dysregulation. The chronic inflammatory state provoked by cytoplasmic DNA sensing mechanisms can deleteriously influence organismal longevity. This nexus between impaired DNA repair, innate immune signaling, and aging trajectories represents a paradigm shift in understanding age-associated diseases and genetic disorders marked by genomic maintenance defects.

Prof. Ðikić emphasizes the significance of this conceptual advance, noting that while Ruijs-Aalfs syndrome exemplifies the clinical relevance of defective DPC repair, analogous mechanisms may underpin other rare genetic conditions. The study’s insights lay a critical foundation for devising targeted treatments aimed at modulating the cGAS-STING pathway or enhancing DPC resolution to forestall inflammation-mediated tissue damage.

By leveraging rare disease models, this research not only delineates the molecular underpinnings bridging DNA repair deficiencies to immune activation but also enriches the broader understanding of the biology of aging. Such knowledge may inspire innovative interventions to mitigate age-related pathologies and extend healthspan. The integration of molecular genetics, cell biology, and immunology exemplified here heralds a transformative approach to complex human diseases.

Collaborative efforts spanning prominent institutions—including Goethe University, Johannes Gutenberg University Mainz, the German Cancer Research Center, EPFL Lausanne, Charité Berlin, and others—highlight the interdisciplinary commitment to unraveling fundamental mechanisms of DNA damage response and its systemic ramifications. This collective endeavor exemplifies translational science at its most impactful, promising to translate bench discoveries into clinical breakthroughs.

In sum, the elucidation of SPRTN’s role in managing DNA-protein crosslinks and the consequent immunological sequelae exposes a critical vulnerability in cellular homeostasis that affects organismal lifespan and disease susceptibility. Future research inspired by these findings will likely probe detailed molecular interactions within the cGAS-STING axis and explore pharmacological inhibitors to quell detrimental inflammation without compromising genomic defense.

Subject of Research: Animals

Article Title: DNA-Protein crosslinks promote cGAS-STING-driven premature aging and embryonic lethality

News Publication Date: 30-Jan-2026

Web References: 10.1126/science.adx9445

References: Science Journal, DOI: 10.1126/science.adx9445

Image Credits: Institute of Biochemistry II, Goethe University Frankfurt

Keywords: Genetic disorders, Diseases and disorders, Health and medicine, Cell biology, Cell proliferation, Nuclear localization, Genetics, Human genetics, Molecular genetics, DNA damage, DNA damage responses, DNA repair, DNA replication, Mutation, Loss of function mutations

Fine particulate matter, specifically PM2.5, refers to airborne particles with a diameter of less than 2.5 micrometers. These particles are notorious for their ability to penetrate deep into the respiratory tract, inciting inflammation and oxidative stress not only in lungs but also in other organs, including the skin. Skin, as the largest and most externally exposed organ, bears the brunt of such environmental insults. PM2.5 exposure leads to enhanced oxidative stress, disrupts cellular homeostasis, and triggers programmed cell death (apoptosis), which collectively accelerate skin aging and exacerbate dermatological conditions. The critical question researchers sought to answer was whether natural compounds could intervene and blunt the cascade of skin damage initiated by PM2.5 exposure.

The focus on Vaccinium oldhamii fruit extract arose from its rich polyphenolic and antioxidant profile, which is historically recognized for medicinal and nutritional benefits. Polyphenols, a group of naturally occurring organic compounds, possess potent antioxidant properties. They scavenge reactive oxygen species (ROS) generated during oxidative stress, thereby preventing macromolecular damage at the DNA, protein, and lipid levels. The study’s approach involved isolating ethanol extracts from the fruits and testing their efficacy on cultured human keratinocytes, the predominant cell type in the outer skin layer, which serves as the first line of defense against environmental damage.

A critical discovery was that ethanol extract of Vaccinium oldhamii effectively reduced PM2.5-induced oxidative stress in keratinocytes by suppressing the overproduction of reactive oxygen species. The excessive ROS generated by particulate matter have long been implicated in damaging cellular mitochondria, disrupting the redox balance, and triggering apoptosis. The data demonstrated that treatment with the fruit extract significantly restored mitochondrial integrity and cellular viability, underscoring a robust antioxidative mechanism that shields keratinocytes from pollutant toxicity.

Interestingly, the study also delved into the interaction between oxidative stress and autophagy processes within skin cells. Autophagy, an evolutionarily conserved cellular mechanism, functions to degrade and recycle damaged organelles and macromolecules, playing a pivotal role in maintaining cellular equilibrium. However, dysregulated autophagy activation in response to PM2.5 can exacerbate cellular stress and trigger apoptosis. The research revealed that Vaccinium oldhamii extract not only quenched oxidative stress but also normalized autophagic activity, preventing excessive autophagy that would otherwise lead to cell death. This dual regulatory role positions the extract as a multifaceted defense agent against environmental stressors.

The implications of this study extend beyond the laboratory bench, offering tangible benefits for public health and dermatological science. Considering the persistent increase in urban air pollution levels worldwide, particularly fine particulate matter, the capacity to counteract skin cell damage naturally could revolutionize topical skincare and preventive dermatology. Vaccinium oldhamii, through its rich bioactive components, emerges as a promising candidate for developing novel cosmeceuticals aimed at protecting skin from pollutant-induced premature aging, inflammation, and barrier dysfunction.

Moreover, antioxidant-based interventions are gaining traction due to their generally favorable safety profiles compared to synthetic agents. The comprehensive biochemical evaluation within this study underscores the ethanol extract’s efficacy coupled with low cytotoxicity, making it suitable for long-term application in skincare formulations. This aligns with current trends emphasizing clean, natural, and efficacious products amid rising consumer demand for sustainable and health-conscious beauty solutions.

The molecular pathways explored in the study provide deeper insights into how environmental toxins mediate damage at the cellular level. By identifying the suppression of PM2.5-induced apoptosis through the inhibition of oxidative stress and excessive autophagy, the research maps critical checkpoints where therapeutic interventions could be targeted. This opens avenues not only for topical protection strategies but also potentially for systemic approaches in preventing pollutant-associated pathologies.

In addition, this research could inspire further exploration into other natural extracts with similar polyphenolic profiles, broadening the scope of natural product pharmacology. Investigating synergistic effects among different plant-derived antioxidants might enhance efficacy and offer multi-targeted protection against complex environmental insults like particulate matter. The protective mechanisms elucidated here serve as a blueprint for future translational research aiming to harness nature’s arsenal against modern health challenges.

The experimental design incorporated rigorous in vitro assays, including cellular viability tests, ROS quantification, mitochondrial membrane potential analysis, and autophagy marker evaluation. This robust methodology ensured that the findings were underpinned by precise biochemical and cellular evidence. The clarity in distinguishing apoptosis from autophagy-related cell death mechanisms further underscores the sophistication and depth of the scientific inquiry.

In the broader context of environmental health sciences, this study contributes to the growing understanding of how chronic exposure to urban air pollutants directly affects skin health, an area historically overshadowed by respiratory and cardiovascular concerns. It emphasizes the skin’s role as not only a barrier but also an active participant in systemic inflammatory and oxidative processes, impacted by external pollutants and modulated by natural antioxidant defenses.

Given the vibrant global research interest in mitigating pollution-related health risks, studies such as this position natural extracts as both therapeutic and preventive tools with practical applications. The bridging of ethnobotanical knowledge with modern molecular biology exemplifies the interdisciplinary approach needed to tackle 21st-century health concerns, blending tradition with innovation.

Finally, as urbanization accelerates and air quality challenges intensify, integrating natural, plant-based extracts with validated protective properties could transform how societies address environmental damage at the individual and communal levels. The Vaccinium oldhamii ethanol extract stands out as a promising ally in this ongoing battle against pollution-induced cellular stress and degeneration, promising a future where nature’s remedies contribute significantly to safeguarding human health.

Subject of Research: Protective effects of ethanol extract of Vaccinium oldhamii fruits on keratinocytes exposed to fine particulate matter (PM2.5), focusing on suppression of oxidative stress and autophagy-mediated apoptosis.

Article Title: Protective effects of ethanol extract of Vaccinium oldhamii fruits against fine particulate matter (PM2.5)-induced apoptosis through suppression of oxidative stress and autophagy activation in keratinocytes.

Article References:
Lee, YH., You, M., Lee, EC. et al. Protective effects of ethanol extract of Vaccinium oldhamii fruits against fine particulate matter (PM2.5)-induced apoptosis through suppression of oxidative stress and autophagy activation in keratinocytes. Food Sci Biotechnol (2025). https://doi.org/10.1007/s10068-025-01983-z

Image Credits: AI Generated

DOI: https://doi.org/10.1007/s10068-025-01983-z

Over the past four decades, Karin’s research journey has been deeply rooted in unraveling the complex molecular mechanisms through which inflammation—a normally protective, acute biological response—turns chronic and pathological. His work elucidates how prolonged, unrelenting inflammation disrupts cellular homeostasis and promotes the development of cancer. At Sanford Burnham Prebys, Karin aims to expand upon these breakthroughs, particularly focusing on metabolic and liver diseases that affect millions worldwide.

Karin’s expertise centers on the intricate signaling pathways that link inflammation to oncogenesis. He is credited with the groundbreaking discovery of the IKK-NF-κB and JNK-AP-1 pathways, two critical molecular cascades that orchestrate inflammatory responses. His seminal work demonstrates how aberrant activation of these pathways disables apoptosis, the programmed cell death process that normally limits uncontrolled cell growth. This evasion of apoptosis is a well-established hallmark of cancer, meaning that chronic inflammation effectively removes critical cellular safeguards and nudges cells toward malignant transformation.

A key facet of Karin’s research trajectory focuses on the interleukin-6 (IL-6) family of cytokines. These signaling molecules, long known for their role in promoting inflammation and autoimmunity, have been shown by Karin to abnormally activate transcription factors that drive gene expression patterns advantageous to cancer development. Specifically, this overactivation contributes to colorectal, liver, and various other malignancies. Furthermore, Karin detailed the pivotal role of the IκB kinase (IKK) complex in facilitating cancer progression through its regulation of the NF-κB transcription factor, highlighting the dual roles of inflammation and immune modulation in tumor biology.

Throughout his career, Karin has been recognized by numerous prestigious awards that underscore the foundational impact of his research. He is a laureate of the AACR G.H.A. Clowes Award for Outstanding Basic Cancer Research and the William B. Coley Award for Distinguished Research in Basic and Tumor Immunology, among others. His election to esteemed scientific bodies including the U.S. National Academy of Sciences, National Academy of Medicine, and the AACR Academy further cements his status as a towering figure in biomedical research.

The timing of Karin’s new leadership at the Center for Metabolic and Liver Diseases is especially pertinent given the rising global health burden posed by metabolic syndromes. In the United States alone, approximately one-third of adults suffer from metabolic syndrome—a constellation of conditions that significantly increase the risk for coronary heart disease, stroke, and type 2 diabetes. Complementing this, liver disease prevalence is staggering; an estimated 30% of U.S. adults have metabolic dysfunction-associated steatotic liver disease (MASLD), and a subset of 5-10% progress to its severe form, metabolic dysfunction-associated steatohepatitis (MASH). These conditions predispose patients to cirrhosis, liver cancer, and eventual organ failure, underscoring the urgent need for effective therapeutic strategies.

Under Karin’s stewardship, the center integrates seven laboratories with complementary expertise ranging from intracellular molecular signaling and translational metabolic research to human physiological studies and clinical trials. This multidisciplinary approach aims to decode the pathological processes that underpin metabolic liver diseases and to drive the innovation of novel therapeutics. Current treatment options for MASLD and MASH remain limited and largely ineffective, highlighting the transformative potential of Karin’s research agenda to impact patient outcomes on a broad scale.

Beyond his administrative role, Karin actively contributes to a major multimillion-dollar Program Project Grant awarded by the National Cancer Institute. This grant focuses on the mechanisms by which hypernutrition and metabolic stress promote the development of non-alcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (HCC). Specifically, Karin investigates the transcription factor NRF2 and the gluconeogenic enzyme FBP1, both implicated in metabolic liver disease progression to liver cancer, positioning his work at the cutting edge of metabolic oncology.

Karin’s scholarly output is formidable, comprising hundreds of peer-reviewed publications published in esteemed journals such as Nature, Cell, Science, Cancer Cell, and Immunity. His research has been cited over 360,000 times, with an h-index of 284, reflecting both the breadth and impact of his contributions to science. Collaborative efforts with colleagues at Sanford Burnham Prebys and beyond amplify the translational potential of his discoveries, ensuring that his insights translate into clinical innovations.

The scientific community and healthcare ecosystem alike stand to benefit from Karin’s leadership as he navigates the complex, intertwined pathways of inflammation, metabolism, and cancer. By advancing mechanistic understanding and spearheading translational research, the newly minted Center for Metabolic and Liver Diseases positions itself as a beacon of hope for tackling some of today’s most pressing and complex health challenges.

Karin’s vision is unequivocal: to develop interventions that can prevent the onset of MASLD and intercept its progression to severe liver disease and cancer. This goal aligns with a broader public health imperative to reduce healthcare costs and improve patient quality of life in the face of metabolic disorders—a burden that continues to escalate globally.

As Michael Karin takes the helm at Sanford Burnham Prebys, the intersection of metabolic dysfunction and oncology research is poised for unprecedented growth. His expertise in dissecting molecular signaling pathways that govern inflammation-mediated cancer biology stands to transform how the scientific community approaches metabolic and liver diseases, opening avenues for innovative therapies that address root causes rather than mere symptoms.

With this appointment, Sanford Burnham Prebys fortifies its status as a vanguard institution in biomedical research, attracting talent capable of bridging fundamental science with clinical application. The Center for Metabolic and Liver Diseases under Karin’s guidance is ready to lead the charge towards new diagnostics, targeted treatments, and ultimately, better patient outcomes in the era of precision medicine.

Subject of Research: Chronic inflammation, metabolic and liver diseases, cancer biology, signaling pathways, metabolic syndrome, and therapeutic development.

Article Title: Michael Karin Takes Helm at Sanford Burnham Prebys to Tackle Chronic Inflammation and Metabolic Liver Disease

News Publication Date: June 30, 2025

Web References:

• https://sbpdiscovery.org/research/centers/center-for-metabolic-and-liver-diseases/
• https://sbpdiscovery.org/scientists/david-a-brenner-md/
• https://sbpdiscovery.org/scientists/peter-d-adams-phd/
• https://sbpdiscovery.org/scientists/randal-j-kaufman-phd/
• https://sbpdiscovery.org/scientists/debanjan-dhar-phd/

Image Credits: Sanford Burnham Prebys

Keywords: Metabolic syndrome, Fatty liver disease, Steatohepatitis, Obesity, Metabolic disorders, Cancer research, Oncology, Liver cancer

At the cellular and molecular levels, the skin exhibits intricate hallmarks of aging that are strikingly interconnected with systemic aging pathways. Chronic exposure to ultraviolet radiation, pollution, and other environmental factors instigates oxidative stress, DNA damage, and inflammatory signaling cascades within dermal and epidermal compartments. These localized stressors propagate systemic effects by disrupting cellular homeostasis and triggering immune dysregulation. The resulting feedback loops amplify senescence-associated phenotypes across tissues, underscoring the bidirectional dialogue between the skin’s microenvironment and broader organismal aging. Understanding these communication networks is imperative to elucidate how skin aging accelerates biological decline beyond its visible manifestations.

One of the pivotal mechanisms through which the skin mediates systemic aging involves the modulation of senescent cell populations. Senescent cells accumulate in both the skin and internal organs with advancing age, secreting a plethora of pro-inflammatory cytokines, growth factors, and matrix-degrading enzymes collectively known as the senescence-associated secretory phenotype (SASP). This paracrine signaling reprograms neighboring cells, perpetuates low-grade chronic inflammation, and contributes to tissue dysfunction. Environmental stressors exacerbating this accumulation in the skin can therefore indirectly fuel systemic inflammatory states linked to age-related diseases such as cardiovascular dysfunction, neurodegeneration, and metabolic disorders. These insights prompt the exploration of senescence-targeted therapeutics as a unified strategy for skin and systemic rejuvenation.

Further complicating the skin-exposome-aging axis is the complex remodeling of the extracellular matrix (ECM), a dynamic scaffold providing structural integrity and biochemical cues for cellular behavior. Environmental insults accelerate ECM degradation through the enhanced activity of matrix metalloproteinases, leading to loss of skin elasticity, impaired barrier function, and altered mechanotransduction. These structural deteriorations not only affect cutaneous architecture but also perturb cellular signaling pathways that regulate systemic metabolic and immune responses. The degradation products of the ECM may serve as bioactive molecules that influence distant tissues, suggesting a systemic ripple effect initiated at the skin level. Consequently, interventions that preserve ECM homeostasis are attractive targets for both dermatological health and systemic aging mitigation.

The skin microbiome, comprising diverse bacterial, fungal, and viral communities, represents an additional layer of complexity interfacing the environment with host physiology. Dysbiosis induced by environmental exposures can disrupt cutaneous immune equilibrium, promote inflammation, and impair barrier function. Emerging evidence suggests that skin microbiome alterations influence systemic immune tone and metabolic homeostasis through microbial metabolites and immune cell priming, thereby impacting biological aging trajectories. Targeting the skin microbiome through prebiotic, probiotic, or microbiome-derived metabolites offers an intriguing frontier for modulating aging processes both locally and systemically.

At the molecular level, epigenetic modifications in skin cells provide a mechanistic link between environmental exposures and aging phenotypes. DNA methylation, histone modifications, and chromatin remodeling in response to ultraviolet radiation and pollutants alter gene expression profiles associated with cellular senescence, repair capacity, and inflammatory tone. These epigenomic changes are increasingly recognized as biomarkers of biological age and predictors of age-related morbidity. Importantly, the reversibility of certain epigenetic marks engenders hope for interventions aimed at resetting the biological clock within skin cells, thereby influencing systemic aging processes through skin-centered rejuvenation strategies.

Recent advancements in single-cell transcriptomics and proteomics have unraveled the heterogeneity of cellular populations in the skin during aging and environmental stress responses. Fibroblasts, keratinocytes, immune cells, and endothelial cells exhibit distinct aging signatures that modulate tissue homeostasis and repair capacity. The interplay of these cell types orchestrates the skin’s resilience or vulnerability to exposome-induced damage, highlighting the necessity of integrative models to capture the multidimensional aging landscape. These technological breakthroughs facilitate the identification of precise biomarkers and molecular targets for personalized anti-aging therapies that account for individual environmental histories and intrinsic susceptibilities.

The bidirectional communication between the skin and systemic physiological systems extends to neuroendocrine pathways as well. The skin serves as a neuroimmunoendocrine organ capable of sensing environmental cues and mediating systemic stress responses through hormonal and neurotransmitter signaling. Chronic exposome insults can dysregulate these pathways, influencing hypothalamic-pituitary-adrenal axis activity and systemic inflammatory milieu, thereby accelerating the aging process. This neuroendocrine interface accentuates the role of skin health not only in structural integrity but also in orchestrating systemic homeostasis and resilience against age-related decline.

Technological innovations in skin modeling, including organoids, bioengineered skin equivalents, and advanced imaging modalities, are revolutionizing the investigation of exposome-aging interactions. These platforms enable controlled manipulation of environmental variables and in-depth longitudinal monitoring of molecular and cellular aging markers. They provide indispensable tools for preclinical assessment of novel therapeutics targeting skin and systemic aging pathways influenced by the exposome. Moreover, integration with computational and machine learning approaches enhances predictive accuracy for individual susceptibility and treatment outcomes, paving the way for precision geroscience.

Despite significant progress, critical knowledge gaps persist in elucidating the mechanisms linking specific exposome factors with discrete hallmarks of aging in the skin and beyond. The heterogeneity in environmental exposures, genetic backgrounds, and lifestyle factors demands comprehensive longitudinal cohort studies and global collaborations to dissect causal pathways and identify universal versus context-dependent aging modulators. Addressing these challenges will inform effective public health strategies for exposure mitigation, skin health preservation, and biological age deceleration.

From a clinical perspective, the convergence of dermatology and geroscience opens unprecedented opportunities for the identification of reliable biomarkers that reflect both skin and systemic biological age. Novel biomarkers encompassing molecular, cellular, and functional metrics will facilitate early detection of accelerated aging and stratification of individuals at risk for age-related diseases. Importantly, such biomarkers can serve as surrogate endpoints for clinical trials of anti-aging interventions, expediting the translation of basic discoveries into preventive and therapeutic applications.

Therapeutic innovations targeting the skin-exposome-aging axis are rapidly evolving. Strategies under investigation include topical and systemic antioxidants, small molecule senolytics and senomorphics, ECM-modulating compounds, microbiome-targeted therapies, and epigenetic modulators. Combination approaches that address multiple aging hallmarks concurrently hold promise for synergistic benefits. The accessibility of the skin enhances the feasibility of localized delivery systems while enabling systemic monitoring of treatment efficacy. These developments herald a new era where skin health maintenance transcends cosmetic considerations to become a cornerstone of healthy aging interventions.

In parallel, lifestyle modifications aimed at reducing harmful environmental exposures and promoting skin resilience constitute a pragmatic approach to decelerate biological aging. Sun protection, pollution avoidance, balanced nutrition, and stress management collectively bolster skin barrier function and systemic homeostasis. Public awareness campaigns and policy initiatives addressing environmental determinants of exposome burden are critical complements to biomedical advances, reinforcing a holistic framework for aging interventions.

The exciting intersection between exposome research, skin biology, and systemic aging underscores the immense potential of cross-disciplinary collaborations integrating dermatology, molecular biology, bioinformatics, environmental science, and clinical medicine. Such integrative efforts are vital for unraveling the complexity of aging and translating mechanistic insights into effective interventions that enhance longevity and quality of life.

In conclusion, the skin functions as a sophisticated interface between the external environment and internal physiological systems, embodying a dynamic recorder and mediator of biological aging. The intricate interplay among exposome factors, skin aging hallmarks, and systemic aging phenotypes reveals opportunities for groundbreaking therapeutic strategies and biomarker development. By deepening our understanding of these mechanisms, leveraging cutting-edge technologies, and fostering collaborative research, we edge closer to realizing personalized approaches that safeguard skin health and promote healthy systemic aging, ultimately transforming how we perceive and address the aging process.

Subject of Research:
Interactions between environmental exposures (exposome), skin aging hallmarks, and systemic biological aging, with implications for therapeutic intervention and biomarker development.

Article Title:
Skin health and biological aging

Article References:
Furman, D., Auwerx, J., Bulteau, AL. et al. Skin health and biological aging. Nat Aging (2025). https://doi.org/10.1038/s43587-025-00901-6

Image Credits: AI Generated