ArticleScientific reports2016
IGF-I induces senescence of hepatic stellate cells and limits fibrosis in a p53-dependent manner.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 3 of them syntheses that pooled it.
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The trial behind it
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Who cites it
81 citing papers in PubMed, 3 syntheses or guidelines pooled it, 164 citations in OpenAlex.
- Serum Insulin-Like Growth Factor 1 and the Prognosis of Patients With Advanced Liver Diseases: A Meta-Analysis.Clinical and translational gastroenterology · 2025Pooled it
- Pooled it
- Insulin-like growth factor-1 and non-alcoholic fatty liver disease: a systemic review and meta-analysis.Endocrine · 2019Pooled it
- Relationship of IGF-1 and IGF-Binding Proteins to Disease Severity and Glycemia in Nonalcoholic Fatty Liver Disease.The Journal of clinical endocrinology and metabolism · 2021Trial
- Effects of tesamorelin on hepatic transcriptomic signatures in HIV-associated NAFLD.JCI insight · 2020Trial
- Acromegaly and Metabolic Dysfunction-Associated Steatotic Liver Disease: Clinical and Therapeutic Implications.Current obesity reports · 2026Review
- [Research progress on cellular senescence and liver diseases].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Adult Growth Hormone Deficiency and Metabolic Dysfunction-Associated Steatotic Liver Disease.Current obesity reports · 2026Review
- Cellular senescence in liver diseases: From molecular drivers to therapeutic targeting.Journal of hepatology · 2026Review
- Growing Pains: GH-induced Fibrosis Across Multiple Organs in bGH Mice.Endocrinology · 2025Article
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease Complicated by Diabetes: Pathophysiology and Emerging Therapies.Journal of obesity & metabolic syndrome · 2025Review
- The context-dependent effect of cellular senescence: From embryogenesis and wound healing to aging.Ageing research reviews · 2025Review
- Advanced Microbiome Therapeutics Accelerate MASLD Recovery by Restoring Intestinal Microbiota Equilibrium and the Gut-Liver Axis in a Mouse Model.Journal of agricultural and food chemistry · 2025Article
- Aging and metabolic dysfunction-associated steatotic liver disease: a bidirectional relationship.Frontiers of medicine · 2025Review
- Stem cell-based therapeutic strategies for liver aging.Liver research (Beijing, China) · 2025Review
- Multiple machine learning algorithms identify 13 types of cell death-critical genes in large and multiple non-alcoholic steatohepatitis cohorts.Lipids in health and disease · 2025Article
- Hypertriglyceridemia and younger age are associated with effectiveness of growth hormone therapy on hepatic steatosis.Endocrine journal · 2025Article
- Risk factors and prediction model of metabolic disorders in adult patients with pituitary stalk interruption syndrome.Scientific reports · 2025Article
- Liver-specific actions of GH and IGF1 that protect against MASLD.Nature reviews. Endocrinology · 2025 · on this mapReview
21 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic fibrosis in nonalcoholic steatohepatitis (NASH) and cirrhosis determines patient prognosis; however, effective treatment for fibrosis has not been established. Oxidative stress and inflammation activate hepatic stellate cells (HSCs) and promote fibrosis. In contrast, cellular senescence inhibits HSCs' activity and limits fibrosis. The aim of this study was to explore the effect of IGF-I on NASH and cirrhotic models and to clarify the underlying mechanisms. We demonstrate that IGF-I significantly ameliorated steatosis, inflammation, and fibrosis in a NASH model, methionine-choline-deficient diet-fed db/db mice and ameliorated fibrosis in cirrhotic model, dimethylnitrosamine-treated mice. As the underlying mechanisms, IGF-I improved oxidative stress and mitochondrial function in the liver. In addition, IGF-I receptor was strongly expressed in HSCs and IGF-I induced cellular senescence in HSCs in vitro and in vivo. Furthermore, in mice lacking the key senescence regulator p53, IGF-I did not induce cellular senescence in HSCs or show any effects on fibrosis. Taken together, these results indicate that IGF-I induces senescence of HSCs, inactivates these cells and limits fibrosis in a p53-dependent manner and that IGF-I may be applied to treat NASH and cirrhosis.
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