ReviewJournal of hepatology2026
Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.
Review in Journal of hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed.
- Retrorsine impairs liver regeneration by inducing progenitor cell-senescenceAnnals of medicine · 2026Article
- Article
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Integrating Structural Characterization, Network Pharmacology, and Experimental Validation Reveals the Anti-Liver Aging Mechanism of Acorus tatarinowii Polysaccharides.Chemistry & biodiversity · 2026Article
- Context-dependent duality of senescent cells in liver fibrosis.Liver research (Beijing, China) · 2026Review
- Molecular mechanisms and pathogenesis of MASH.Nature · 2026Review
- Senescence-Related SOCS1, SOCS2, and GADD45G Identify an Immune-Associated Molecular Signature in Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomolecules · 2026Article
- Review
- Integrated bioinformatic evaluation unveils a cellular senescence gene signature as a poor prognostic factor in hepatocellular carcinoma.Clinical and experimental medicine · 2026Article
- Gut Microbiota and Ageing: A Critical Crosstalk in Alcohol-Related Liver Disease.Microorganisms · 2026Review
- Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review.Proteomes · 2026Review
- [Research progress on cellular senescence and liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Review
- Marine Bioactives in Liver Aging: Mechanistic Insights and Translational Potential.Marine drugs · 2026Review
- A machine learning-derived biological age model for liver grafts provides a superior assessment of aging compared to chronological age in transplantation.Scientific reports · 2026Article
- Toll-like receptor 2 drives liver senescence and fibrosis in aging through gut-derived microbial signaling.Cellular & molecular biology letters · 2026Article
- Multiomics analysis reveals that senescent CXCL16Journal of translational medicine · 2026Article
- The Interplay Between Cellular Senescence and Lipid Metabolism in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).International journal of molecular sciences · 2026Review
- The Biological Mechanisms of Frailty: Focusing on Cellular Senescence.European cardiology · 2026Review
- Integrating senotherapeutics into transplantation: liver reconditioning in an aging donor pool.Transplant international : official journal of the European Society for Organ Transplantation · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Obesity, metabolic syndrome, and aging are major contributors to the rising global burden of chronic liver diseases. Among these, aging remains an often underrecognised driver that intersects with other metabolic and environmental insults to exacerbate liver dysfunction. Cellular senescence, a key hallmark of aging, is increasingly implicated as a central mechanism linking these risk factors to liver pathophysiology. Senescent cells accumulate across diverse hepatic cell types and influence disease progression and systemic health through their SASP (senescence-associated secretory phenotype). While senotherapeutic strategies, including senolytics and senomorphics, show promise, their efficacy and safety remain highly dependent on cell type, disease context, and agent specificity. Recent advances, such as multi-omics profiling, multi-marker gene signatures, and targeted modalities including PROTACs (proteolysis targeting chimeras) and CAR (chimeric antigen receptor) T-cell therapies, offer new opportunities for precision interventions. This review synthesises emerging insights into the molecular mechanisms of liver senescence, evaluates the current landscape of senotherapies, and outlines key challenges and future directions for safely and effectively targeting senescence in chronic liver disease.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.