The study, led by M.A.J. Morsink, S. Fleischer, T.R. Nash and colleagues, presents what it describes as a practical toolbox for modelling fibrosis outside the body. Rather than treating fibrosis as a single disease, the authors examine the biological features shared across organs while recognizing that each tissue has its own cellular composition, mechanical environment and response to injury. This distinction is critical. A model that reproduces collagen accumulation in a dish may still fail to capture the electrical properties of the heart, the air–liquid interface of the lung, the filtration architecture of the kidney or the specialized immune environment of the liver. Faithful modelling therefore requires more than adding a profibrotic chemical to cultured cells.

At the centre of fibrosis is a complex interaction between injured parenchymal cells, immune cells, vascular cells and fibroblasts. Fibroblasts are connective-tissue cells that normally help maintain the extracellular matrix and support wound healing. During chronic injury, however, they can become activated into myofibroblasts, contractile cells that produce large quantities of collagen and other matrix proteins. Signalling molecules such as transforming growth factor beta are widely associated with this transition, but fibrosis is not controlled by one pathway alone. Cytokines, growth factors, oxidative stress, altered metabolism and signals from damaged cells can all contribute. The review emphasizes that in vitro systems should reproduce this multicellular communication rather than isolate a single cell type from its biological context.

The extracellular matrix itself is not simply a passive scar. Its composition, organization and physical properties can actively direct cell behaviour. As collagen and related proteins accumulate, the tissue becomes stiffer. That mechanical change can activate mechanosensitive pathways, including signalling through integrins and transcriptional regulators such as YAP and TAZ. In turn, cells may produce even more matrix, creating a self-reinforcing cycle in which biochemical and mechanical signals amplify one another. A useful fibrosis model must therefore measure not only the quantity of deposited matrix but also its organization, crosslinking, stiffness and ability to alter cellular function. Techniques such as three-dimensional biomaterials, tunable hydrogels, traction-force measurements and advanced microscopy can help investigators observe these changes in real time.

The authors identify three-dimensional human tissue models as an important bridge between conventional cell culture and animal studies. Two-dimensional cultures are relatively inexpensive and experimentally convenient, but they flatten cells onto artificial surfaces and often expose them to conditions unlike those found in living tissue. Three-dimensional systems can allow cells to adopt more realistic shapes, form tissue-like interfaces and experience gradients of oxygen, nutrients and signalling molecules. Organoids, engineered tissue constructs and organ-on-chip platforms can further introduce fluid flow, vascular-like channels or mechanical stimulation. These features may be especially valuable for modelling organs in which physical forces are central to disease, such as the breathing lung, the beating heart and the continuously perfused kidney.

Human cells are another major advantage of these systems. Primary cells obtained from patients can retain disease-associated characteristics, while induced pluripotent stem cells can be differentiated into several human cell types and combined into more complex models. Patient-derived material may reveal why some individuals develop aggressive fibrosis after injury while others recover with limited scarring. It may also expose differences in drug response that are invisible in genetically uniform laboratory animals or immortalized cell lines. Yet the review cautions that human relevance does not automatically guarantee biological accuracy. Cells can lose their identity during expansion, stem-cell-derived populations may remain immature and donor-to-donor variability can make results difficult to compare. Rigorous characterization is therefore essential.

A major design challenge is deciding which hallmarks of fibrosis a model must reproduce. The review proposes that researchers begin with the biology of the target organ and define measurable criteria before selecting a platform. These criteria may include persistent fibroblast activation, pathological extracellular matrix deposition, tissue stiffening, inflammatory signalling, altered vascular behaviour, epithelial or endothelial dysfunction and loss of organ-specific performance. In a lung model, for example, meaningful fibrosis should involve more than collagen production; it should also reflect changes in epithelial integrity, gas-exchange-related functions and the interaction between airway or alveolar cells and immune populations. In a cardiac model, contractility and electrical activity may be as important as matrix accumulation.

The practical value of a model depends equally on how its results are measured. Traditional endpoint assays can quantify collagen or profibrotic gene expression, but they may miss changes that emerge earlier or disappear by the time a sample is collected. The authors highlight the growing importance of live imaging, single-cell and spatial molecular profiling, secreted-protein analysis, mechanical testing and functional readouts. Combining these methods can reveal which cells initiate fibrosis, how signals move through a tissue and whether a treatment reverses disease-associated function rather than merely suppressing one marker. Standardized reporting of cell sources, matrix composition, culture conditions, disease induction methods and analysis pipelines will also be necessary if results from different laboratories are to be compared.

These models could reshape the search for antifibrotic therapies, a field in which promising laboratory findings have often failed to translate into durable clinical benefits. A well-designed human tissue system could be used to test candidate drugs across several stages of disease, from early inflammatory activation to established matrix remodelling. It might also help distinguish compounds that genuinely restore tissue function from those that simply reduce a biomarker. Because fibrosis frequently involves multiple cell types and feedback loops, future platforms may be particularly useful for evaluating drug combinations and identifying patients most likely to respond. The authors ultimately present in vitro fibrosis modelling not as a replacement for clinical or animal research, but as a complementary technology capable of narrowing the gap between molecular discovery and human disease.

The review’s broader message is that the next generation of fibrosis models should be designed as integrated biological systems rather than as collections of isolated measurements. Researchers will need to combine human cells, organ-specific architecture, immune interactions, extracellular-matrix biology, mechanical forces and functional outputs in a manner that remains experimentally manageable. Advances in microfluidics, biomaterials, imaging and computational analysis could make such systems increasingly precise, while shared standards may improve reproducibility and accelerate adoption beyond specialist laboratories. By defining the hallmarks that matter most and translating them into practical design choices, the authors offer a framework for building models that are not only technically sophisticated but clinically informative. For a disease responsible for progressive organ failure across the world, that shift could turn the laboratory dish into a more powerful window on how scarring begins, persists and might finally be stopped.

Subject of Research: Human in vitro models of fibrosis across multiple organs, including the heart, lung, kidney, liver and synovium.

Article Title: A practical toolbox for modelling fibrosis in vitro

Article References: Morsink, M.A.J., Fleischer, S., Nash, T.R. et al. A practical toolbox for modelling fibrosis in vitro. Nature Biomedical Engineering (2026). https://doi.org/10.1038/s41551-026-01749-w

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DOI: https://doi.org/10.1038/s41551-026-01749-w

Keywords: Fibrosis, in vitro models, tissue engineering, extracellular matrix, organoids, organ-on-chip, mechanobiology, human disease modelling, drug discovery, regenerative medicine.

Fibrosis, characterized by excessive deposition of extracellular matrix components, notably collagen, culminates in tissue scarring and organ dysfunction. Transforming growth factor-beta (TGF-β) is widely recognized as a master regulator in the fibrotic cascade, orchestrating cellular and molecular events that lead to pathological tissue remodeling. Despite extensive investigation into the TGF-β pathway, the metabolic underpinnings that contribute to fibrotic progression have remained elusive until now.

The research team, led by Meliton et al., meticulously dissected the metabolic landscape within cells responding to TGF-β stimulation. Their data reveal that mitochondrial one-carbon metabolism—a complex biochemical route traditionally associated with nucleotide biosynthesis and methylation reactions—is critically required for the synthesis of glycine, a central amino acid implicated in collagen production. This connection between mitochondrial metabolism and fibrotic signaling highlights a sophisticated metabolic requirement underpinning the fibrotic phenotype.

One-carbon metabolism encompasses a network of interrelated pathways that transfer single-carbon units for the biosynthesis of vital biomolecules. In the mitochondria, key enzymes orchestrate the generation of one-carbon donors, notably through the folate cycle, which is intricately linked to amino acid metabolism. The study demonstrates that disrupting mitochondrial one-carbon pathways impairs glycine production and, consequently, hinders the TGF-β-driven fibrotic program.

Glycine’s integral role in collagen composition—accounting for approximately one-third of the amino acids in collagen—renders this amino acid vital for extracellular matrix assembly during fibrosis. By elucidating how mitochondrial metabolism fuels glycine biosynthesis, the study shifts focus from mere signaling cascades to metabolic substrates, suggesting that metabolic modulation could stymie the fibrotic process.

Methodologically, the research combined state-of-the-art metabolic flux analyses, genetic manipulation of mitochondrial enzymes, and rigorous phenotypic assays to authenticate their claims. The authors employed isotope tracing to map the trajectory of carbon atoms through metabolic pathways, confirming that mitochondrial one-carbon units are channeled specifically towards glycine synthesis upon TGF-β activation. Such metabolic tracing techniques provide unprecedented insight into dynamic cellular processes that underpin pathological states.

Importantly, the findings highlight that the blockade of mitochondrial one-carbon metabolism attenuates fibrotic responses both in vitro and in vivo, implying tangible translational potential. Pharmacological inhibition or genetic silencing of key mitochondrial enzymes involved in one-carbon metabolism significantly reduced collagen deposition and fibrosis markers in animal models, underscoring the therapeutic promise of targeting this metabolic axis.

The broader implications of this research impact our conceptual framework of fibrotic disease biology. By demonstrating that mitochondrial metabolism is not a mere background player but a critical determinant of TGF-β-induced fibrosis, the study bridges metabolism and signal transduction, encouraging a holistic perspective that integrates bioenergetics with molecular signaling.

Furthermore, this metabolic insight could inspire novel pharmacological strategies. Existing antifibrotic therapies have limited efficacy and often come with substantial side effects. Targeting mitochondrial one-carbon metabolism may offer a more precise intervention point, potentially alleviating pathological fibrosis without hampering physiological functions reliant on TGF-β signaling.

The discovery also prompts questions about metabolic plasticity in fibrotic cells. It would be essential to understand how changes in mitochondrial dynamics and one-carbon metabolism influence different stages of fibrosis and whether these pathways interact with other metabolic alterations observed in diseased tissues. Such knowledge could refine patient stratification and treatment personalization.

Moreover, the work hints that mitochondrial health and bioenergetics are deeply intertwined with cellular remodeling processes. Fibrosis has traditionally been viewed through the prism of cytokine signaling and extracellular matrix regulation; however, this research advocates for the inclusion of mitochondrial metabolism as a central axis in disease progression narratives.

This study exemplifies the power of systems biology approaches that combine metabolic profiling, molecular biology, and animal modeling to unravel complex disease mechanisms. Integrating these disciplines is becoming increasingly vital for decoding multifactorial diseases like fibrosis, where signaling and metabolism converge to drive pathogenesis.

In conclusion, the elucidation of mitochondrial one-carbon metabolism as a requisite for TGF-β-driven glycine production and fibrotic responses marks a significant advancement in the field. It redefines our molecular understanding of fibrosis and spotlights metabolism as a fertile ground for therapeutic innovation. With this new paradigm, researchers and clinicians are better equipped to develop targeted strategies aimed at mitigating fibrotic burden, ultimately improving outcomes for patients plagued by chronic fibrotic diseases.

As future research builds on these findings, the scientific community anticipates that metabolic interventions will complement or even surpass existing antifibrotic treatments. Success in this arena could herald a new era in managing fibrosis, transforming it from a difficult-to-treat condition into one that is metabolically controllable and reversible.

Subject of Research:
The study investigates the role of mitochondrial one-carbon metabolism in TGF-β-induced glycine synthesis and fibrotic responses.

Article Title:
Mitochondrial one-carbon metabolism is required for TGF-β-induced glycine synthesis and fibrotic responses

Article References:
Meliton, A.Y., Shin, K.W.D., Cetin-Atalay, R. et al. Mitochondrial one-carbon metabolism is required for TGF-β-induced glycine synthesis and fibrotic responses. Nat Commun 16, 9250 (2025). https://doi.org/10.1038/s41467-025-64320-2

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Liver fibrosis, a hallmark of chronic liver injury, involves complex cellular and molecular dynamics culminating in excessive extracellular matrix deposition and architectural distortion. While cholestasis—characterized by impaired bile flow—is a principal driver of fibrosis, the molecular mechanisms engaged especially in liver parenchyma not directly obstructed by bile remain elusive. This ambiguity has long posed challenges for targeted interventions, as traditional models have conflated global liver injury with localized fibrogenesis. The sBDL model addresses this by inducing bile duct ligation in specific liver segments, effectively mimicking segmental cholestasis and preserving other regions free from obstruction.

Researchers used the sBDL model to investigate the fibrotic response within both obstructed (BO) and unobstructed (WBO) parenchyma, analyzing gene expression patterns alongside detailed histological assessments. This dual approach unveiled a complex landscape where fibrogenic signals are not confined to the areas of obstruction but extend to neighboring parenchyma through poorly understood pathways. Intriguingly, the study reveals that non-obstructed regions exhibit distinctive molecular profiles that indicate active fibrogenic mechanisms, challenging prior assumptions that these areas remain inert in the context of segmental cholestasis.

Central to these revelations is the identification of key regulatory genes implicated in hepatic fibrogenesis across BO and WBO zones. The data demonstrate differential expression of genes involved in extracellular matrix production, inflammatory signaling, and cellular stress responses. The upregulation of profibrotic mediators such as transforming growth factor-beta (TGF-β) and connective tissue growth factor (CTGF) in both regions underscores a systemic hepatic reaction rather than a restricted focal injury. Moreover, immune-modulatory pathways involving cytokines and chemokines appear to orchestrate fibrogenic cascades beyond the immediate area of bile duct obstruction.

Histopathological examinations provided striking visual confirmation of fibrosis hallmarks. In BO parenchyma, classical features including bile duct proliferation, portal inflammation, and collagen deposition were robustly evident. However, even WBO segments displayed subtle yet significant fibrotic remodeling, marked by interstitial matrix accumulation and mild inflammatory infiltrates. These histological nuances affirm that molecular perturbations translate into structural changes, emphasizing a continuum of fibrogenic activity extending across hepatic territories regardless of direct bile flow impairment.

A particularly fascinating aspect of this research lies in the temporal evolution of fibrogenesis within the sBDL framework. By tracking gene expression and histological dynamics over time, the study delineates a progression from early inflammatory signaling to chronic fibrotic remodeling. The initial immune cell activation within obstructed segments triggers paracrine effects that seemingly prime adjacent unobstructed tissue toward a fibrogenic phenotype. This spillover phenomenon elucidates how segmental cholestasis propagates hepatic injury, revealing a ripple effect that defies strict anatomical boundaries.

The implications for pediatric hepatology are profound, especially considering that the sBDL model was applied in weaned rats, reflecting a developmental stage correlating with infancy and early childhood in humans. Pediatric cholestatic diseases, such as biliary atresia, often involve segmental fibrotic lesions that evolve unpredictably. Understanding the molecular dialogues governing fibrosis both within and beyond obstructed zones could inform the timing and targets of interventions aiming to arrest or reverse scarring in young patients.

Beyond the identification of candidate genes, the study leveraged advanced transcriptomic analyses to map entire signaling networks activated during fibrogenesis. This systems biology perspective revealed cross-talk between hepatic stellate cells, biliary epithelial cells, and immune populations like macrophages and T cells. Such interactions create a microenvironment conducive to sustained matrix deposition and tissue remodeling. Targeting these cellular conversations holds promise for novel antifibrotic drugs that could disrupt the pathogenic feedback loops maintaining chronic liver damage.

The selective nature of bile duct ligation in this model also provides unparalleled specificity to discern localized versus systemic effects within the liver. Unlike global bile duct ligation, which induces widespread cholestasis and complicates interpretation, sBDL confines obstruction to anatomically defined lobes. This precision not only enhances experimental reproducibility but also mirrors clinical scenarios where segmental bile duct injuries or obstructions predominate. Therefore, the translational value of these findings is particularly high.

Importantly, the study’s methodology integrated rigorous quantitative histology with state-of-the-art molecular assays, such as RNA sequencing and immunohistochemistry. This multidisciplinary approach ensured that observed gene expression shifts corresponded with tangible tissue alterations. The congruence between molecular data and histopathological evidence strengthens the validity of the proposed mechanisms, establishing a robust framework for subsequent functional studies aimed at intervention development.

Furthermore, the elucidation of WBO parenchyma fibrogenesis opens a new frontier in liver research, challenging the convention that fibrosis is confined to zones of direct injury. The demonstration that seemingly unaffected regions undergo molecular changes indicative of fibrogenesis suggests that current clinical assessments may underestimate the true extent of hepatic involvement in cholestatic diseases. This insight calls for enhanced diagnostic modalities capable of detecting early fibrotic changes beyond visibly affected areas.

In sum, this pioneering investigation into segmental cholestasis via the sBDL model uncovers a nuanced hepatic fibrogenic landscape, emphasizing the interplay between obstructed and unobstructed parenchymal regions. By highlighting key profibrotic genes, temporal dynamics, and intercellular signaling networks, the research sets the stage for innovative therapeutic strategies designed to intercept fibrogenesis before irreversible cirrhosis ensues.

As the global burden of liver fibrosis continues to climb, propelled by diverse etiologies including cholestasis, metabolic syndrome, and viral infections, scientific breakthroughs such as this offer a beacon of hope. The ability to parse fibrotic progression at the molecular level not only aids in identifying novel drug targets but also refines prognostic capabilities. Ultimately, translating these insights into clinical interventions may revolutionize how chronic liver diseases are managed, especially among vulnerable pediatric populations.

This study exemplifies the power of precision modeling combined with comprehensive molecular profiling to unravel complex disease processes. Future research building on these findings will likely explore the reversibility of WBO-induced fibrogenesis, potential regenerative therapies, and application in human liver disease contexts. The promise of tailored, segment-specific treatments for cholestatic fibrosis now appears within reach, ushering in a new era of hepatology innovation.

Subject of Research: Molecular and histopathological characterization of hepatic fibrogenesis after segmental cholestasis using the selective bile duct ligation model in weaned rats.

Article Title: Key genes and histopathological alterations in hepatic fibrogenesis after segmental cholestasis in weaned rats.

Article References:
Gonçalves, J.O., Mafra, C.A.M., Castro, I.d. et al. Key genes and histopathological alterations in hepatic fibrogenesis after segmental cholestasis in weaned rats. Pediatr Res (2025). https://doi.org/10.1038/s41390-025-04272-x

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DOI: https://doi.org/10.1038/s41390-025-04272-x

Liver fibrosis, characterized by excessive deposition of extracellular matrix components, leads to the disruption of normal hepatic architecture and function. Central to this process is the phenomenon of capillarisation, where specialized fenestrated LSECs lose their unique morphology and transform into a continuous, capillary-like endothelium. This transformation impairs the highly selective filtration function of LSECs, contributing to the progression of liver fibrosis and, ultimately, cirrhosis. Understanding and reversing this capillarisation have been long-standing objectives, as the restoration of LSEC function could halt or even reverse fibrotic progression.

The research team led by Liu, W., Liu, Y., and Zhang, L. engineered nucleic acid-based spherical nanoparticles designed to intervene in the cellular pathways that govern LSEC capillarisation. Unlike conventional small molecules or antibody therapies, these nucleic acid spheres offer a multifaceted mechanism of action: they can be programmed to deliver specific sequences capable of modulating gene expression, interfering with pathological signaling cascades, and promoting cellular reversion to a healthy phenotype. Their unique spherical configuration enhances stability and cellular uptake, bypassing many shortcomings encountered by traditional nucleic acid therapies.

At the molecular level, it is well understood that capillarisation is driven by aberrant activation of pro-fibrotic signaling pathways, including those mediated by transforming growth factor-beta (TGF-β), vascular endothelial growth factor (VEGF), and Notch signaling. These pathways collectively promote endothelial dedifferentiation, loss of fenestrae, and basement membrane deposition. The nucleic acid spheres are designed to target key molecules within these signaling networks, thereby attenuating fibrotic signaling and restoring the fenestrated phenotype characteristic of healthy LSECs.

A particularly novel aspect of Liu et al.’s strategy is the ability of nucleic acid spheres to penetrate the liver sinusoidal environment efficiently. The unique size and surface chemistry of these spheres facilitate their selective uptake by LSECs, minimizing off-target effects and potential systemic toxicities. This selective targeting is crucial, considering the liver’s complex cellular heterogeneity and the unique fenestrated morphology that defines LSECs. Effective delivery to these cells has previously been a formidable barrier to therapeutic development.

Their in vitro experiments demonstrated remarkable efficacy in reversing capillarisation markers in cultured LSECs subjected to fibrotic stimuli. Upon treatment with nucleic acid spheres, LSECs exhibited restored fenestrae structures, reduction in basement membrane proteins, and downregulation of endothelial-to-mesenchymal transition markers. These morphological and molecular changes indicate a functional reversion towards a healthy endothelium, an encouraging endpoint rarely achieved by previous interventions.

Moving beyond cell culture, the team validated their approach in murine models of liver fibrosis induced by carbon tetrachloride and bile duct ligation. Systemic administration of nucleic acid spheres resulted in significant improvements in liver histology, marked decreases in collagen deposition, and restored endothelial fenestration as assessed by electron microscopy. Functional assays revealed improved hepatic perfusion and metabolic function, linking the morphological restoration directly to improved liver physiology.

The implications of this study extend well beyond the realm of experimental therapeutics. By showcasing the potential of nucleic acid nano-constructs as precise modulators of endothelial function, Liu et al. open avenues for addressing a wide range of vascular pathologies characterized by endothelial dysfunction. Importantly, these spheres are customizable, suggesting a versatile platform that can be adapted for various disease contexts, including other fibrotic diseases, vascular malformations, and perhaps even tumor vasculature normalization.

Central to the success of this approach is the careful design of the nucleic acid spheres to resist nuclease degradation, a major limitation in nucleic acid therapeutics. The authors employed chemical modifications of nucleotides and a controlled self-assembly process to generate spheres stable under physiological conditions. This stability ensures sustained bioavailability and effective biological activity, overcoming a significant hurdle in the translation of nucleic acid therapies.

Another innovation lies in the interactivity of the nucleic acid spheres with the intracellular machinery of LSECs. Beyond delivering inhibitory RNA sequences, these spheres act as scaffolds, recruiting endogenous regulatory proteins that amplify anti-fibrotic signaling. This multi-layered mode of action potentiates therapeutic outcomes, rendering the approach both robust and adaptable.

The safety profile reported by Liu et al. is equally encouraging. Comprehensive toxicology studies showed no significant off-target immune activation, hepatotoxicity, or systemic adverse effects at therapeutically effective doses. Given the immunogenic risk often associated with nanoparticle-based therapies, this finding paves the way for clinical translation, underscoring the biocompatibility of the nucleic acid sphere platform.

Clinical translation remains a critical future step. The team outlines strategies to scale up nucleic acid sphere production under Good Manufacturing Practice (GMP) conditions and plans to initiate early-phase clinical trials targeting patients with early-stage liver fibrosis. If successful, this therapy could shift the treatment paradigm from symptom management to direct disease modification, a transformative advancement in hepatology.

The impact of Liu et al.’s research resonates within the scientific community and beyond. The use of nucleic acid nanotechnology to orchestrate endothelial cell phenotypes represents an elegant convergence of molecular biology, nanomedicine, and vascular biology. It challenges the traditional confines of drug design and opens the playing field for sophisticated biological interventions tuned at the genomic and proteomic levels.

Moreover, the study highlights the importance of targeted delivery in overcoming biological barriers intrinsic to complex organs such as the liver. By refining cellular specificity and enhancing intracellular trafficking, therapeutic nucleic acid spheres embody the next generation of precision medicine aimed at tackling chronic, otherwise intractable diseases.

As liver fibrosis affects millions worldwide, contributing significantly to morbidity and mortality, the potential societal impact of such a therapy is profound. The promise of restoring healthy liver vasculature and halting fibrotic progression could alleviate burdens on healthcare systems and improve patient quality of life on a global scale.

The methodology and findings of Liu and colleagues also inspire future research directions. The utility of nucleic acid spheres could extend to other endothelial subtypes and fibrotic models, and their modular nature suggests integration with emerging gene editing tools, such as CRISPR-Cas systems, to further refine therapeutic precision.

Finally, these findings underscore the essential role of interdisciplinary collaboration in advancing biomedical innovation. The marriage of nucleic acid chemistry, vascular biology, and nanotechnology exemplified in this study demonstrates how convergent science can unlock new therapeutic frontiers.

In conclusion, the therapeutic deployment of nucleic acid spheres to reverse LSEC capillarisation represents a landmark achievement in liver fibrosis research. Liu et al. have charted a course toward restoring endothelial health and tackling fibrosis at its vascular roots. Their work lays a formidable foundation for translating nanomedicine into clinically viable solutions, poised to transform the future landscape of liver disease treatment.

Subject of Research: Treatment of capillarisation of liver sinusoidal endothelial cells in liver fibrosis using nucleic acid spheres

Article Title: Nucleic acid spheres for treating capillarisation of liver sinusoidal endothelial cells in liver fibrosis

Article References:

Liu, W., Liu, Y., Zhang, L. et al. Nucleic acid spheres for treating capillarisation of liver sinusoidal endothelial cells in liver fibrosis.
Nat Commun 16, 4517 (2025). https://doi.org/10.1038/s41467-025-59885-x

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