ArticleScience translational medicine2018
TGFβ inhibition restores a regenerative response in acute liver injury by suppressing paracrine senescence.
Article in Science translational medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.
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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.
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Who cites it
152 citing papers in PubMed, 258 citations in OpenAlex.
- Cell-type-specific damage scores reveal kidney and liver disease trajectories in single-cell and spatial transcriptomics.Cell genomics · 2026Article
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Tumor Treating Fields Enhance Temozolomide-Associated Growth Suppression in Glioblastoma Cells and Patient-Derived Organoids Through Cell-Cycle Blockade, Apoptosis, and SMAD-Associated Signaling.CNS neuroscience & therapeutics · 2026Article
- Senescent Human Liver Endothelial Cells Mediate CD4Immunology · 2026Article
- The Zinc-Senescence Axis in Skin Aging and Wound Healing: A Narrative Review.International journal of molecular sciences · 2026Review
- Exacerbation of neuronal senescence after spinal cord injury: Role of the macrophage-derived transforming growth factor-β1-SMAD2 signaling axis.Neural regeneration research · 2026Article
- Synergistic senolytic-regenerative therapy significantly extends healthspan and lifespan.Journal of translational medicine · 2026Article
- The effects of splenectomy, platelet-rich plasma (PRP) and concentrated growth factor (CGF) on liver regeneration following major hepatectomy in rats.Scientific reports · 2026Article
- Senescent cells in systemic aging: SASP heterogeneity, immune escape, and endocrine modulation.Biogerontology · 2026Review
- Liver progenitor cells perform wound healing in a scratch assay by concerted bistable circuits.NPJ systems biology and applications · 2026Article
- Senescent hepatic stellate cells drive inflammation and disease progression in MASH (Review).Experimental and therapeutic medicine · 2026Review
- Redefining senescence through hepatocyte fate changes in liver diseases.Trends in endocrinology and metabolism: TEM · 2026Review
- The gut as a central hub for multi-organ crosstalk in aging.Cellular and molecular life sciences : CMLS · 2026Review
- Hepatocyte-Specific MET Deletion Exacerbates Acetaminophen-Induced Hepatotoxicity in Mice.The American journal of pathology · 2026Article
- Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Cellular Senescence, Inflammaging and Cardiovascular Disease.Immunological reviews · 2026Review
- Pathological Interplay of ROS With Myofibroblasts: An Impediment to Corneal Restitution.Oxidative medicine and cellular longevity · 2026Review
- Characteristic Changes in the Immune Landscape of Aging Liver: From Basic Mechanism to Clinical Transformation.Journal of immunology research · 2026Review
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Liver regeneration: unraveling the molecular mechanisms and clinical application.Journal of translational medicine · 2025Review
92 more citing papers are in PubMed but not listed here.
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Authors and funding
34 authors at 11 institutions in 7 countries.
Funding
Abstract
Liver injury results in rapid regeneration through hepatocyte proliferation and hypertrophy. However, after acute severe injury, such as acetaminophen poisoning, effective regeneration may fail. We investigated how senescence may underlie this regenerative failure. In human acute liver disease, and murine models, p21-dependent hepatocellular senescence was proportionate to disease severity and was associated with impaired regeneration. In an acetaminophen injury mouse model, a transcriptional signature associated with the induction of paracrine senescence was observed within 24 hours and was followed by one of impaired proliferation. In mouse genetic models of hepatocyte injury and senescence, we observed transmission of senescence to local uninjured hepatocytes. Spread of senescence depended on macrophage-derived transforming growth factor-β1 (TGFβ1) ligand. In acetaminophen poisoning, inhibition of TGFβ receptor 1 (TGFβR1) improved mouse survival. TGFβR1 inhibition reduced senescence and enhanced liver regeneration even when delivered beyond the therapeutic window for treating acetaminophen poisoning. This mechanism, in which injury-induced senescence impairs liver regeneration, is an attractive therapeutic target for developing treatments for acute liver failure.
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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.