ArticleGastroenterology2008
Accumulation of hedgehog-responsive progenitors parallels alcoholic liver disease severity in mice and humans.
Article in Gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 164 citations in OpenAlex.
- Article
- Anti-aging effect of Hedgehog signaling.Experimental & molecular medicine · 2026Review
- Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease: A Multicellular Perspective.The American journal of pathology · 2026Review
- Dysregulated RNA splicing impairs regeneration in alcohol-associated liver disease.Nature communications · 2025Article
- MiRNAs in Alcohol-Related Liver Diseases and Hepatocellular Carcinoma: A Step toward New Therapeutic Approaches?Cancers · 2023Review
- NOTCH signalling - a core regulator of bile duct disease?Disease models & mechanisms · 2023Review
- Recent Updates on Viral Oncogenesis: Available Preventive and Therapeutic Entities.Molecular pharmaceutics · 2023Review
- Indian Hedgehog release from TNF-activated renal epithelia drives local and remote organ fibrosis.Science translational medicine · 2023Article
- Current Therapeutic Options and Potential of Mesenchymal Stem Cell Therapy for Alcoholic Liver Disease.Cells · 2022Review
- Role of mechanistic target of rapamycin in autophagy and alcohol-associated liver disease.American journal of physiology. Cell physiology · 2022Review
- Clinical, histological and molecular profiling of different stages of alcohol-related liver disease.Gut · 2022Observational
- Gypenosides ameliorate ductular reaction and liver fibrosisFrontiers in pharmacology · 2022Article
- Mesenchymal Stem Cells Influence Activation of Hepatic Stellate Cells, and Constitute a Promising Therapy for Liver Fibrosis.Biomedicines · 2021Review
- Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis-Roles as Putative Treatment Targets?Biomedicines · 2021Review
- Review
- Epithelial splicing regulatory protein 2-mediated alternative splicing reprograms hepatocytes in severe alcoholic hepatitis.The Journal of clinical investigation · 2020Article
- Cellular and molecular basis of liver regeneration.Seminars in cell & developmental biology · 2020Review
- Non-canonical Wnt signalling regulates scarring in biliary disease via the planar cell polarity receptors.Nature communications · 2020Article
- Rewiring Host Signaling: Hepatitis C Virus in Liver Pathogenesis.Cold Spring Harbor perspectives in medicine · 2020Review
- Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsImproving outcomes in alcoholic liver disease (ALD) necessitates better understanding of how habitual ethanol (EtOH) consumption alters normal regenerative mechanisms within the liver. Hedgehog (Hh) pathway activation promotes expansion of progenitor populations in other tissues. We evaluated the hypothesis that chronic EtOH exposure activates Hh signaling in liver.
methodsHh signaling, liver progenitors, transforming growth factor (TGF)-beta induction, and liver damage were compared in mice fed chow, high-fat diets (HF), or HF + EtOH for 4 weeks. Susceptibility to TGF-beta-mediated apoptosis was compared in Hh-responsive liver cells (eg, immature cholangiocytes and oval cells) and mature hepatocytes (which are unresponsive to Hh). Hepatic accumulation of Hh-responsive cells were compared in controls and ALD patients and correlated with a discriminant function (DF) that predicts subacute mortality.
resultsHh signaling and numbers of Hh-responsive cells were increased in HF mice and greatest in HF+EtOH mice. In both, progenitor and stromal cell populations harbored Hh-responsive cells. More ductular-type progenitors and fibrosis markers were noted in HF+EtOH mice than in HF mice. The former also expressed more TGF-beta-1. TGF-beta-1 treatment selectively promoted the viability of Hh-responsive immature liver cells and caused mature hepatocytes that survived to produce Hh ligands. Hh-responsive cells were increased in ALD patients. Lobular accumulation of Hh-responsive immature ductular cells was greater in those with a DF >32 than those with a DF <32.
conclusionsHh signaling is increased in ALD and may influence ALD outcomes by promoting hepatic accumulation of immature ductular cells.
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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.