ArticleHepatology (Baltimore, Md.)2010
Disruption of the growth hormone--signal transducer and activator of transcription 5--insulinlike growth factor 1 axis severely aggravates liver fibrosis in a mouse model of cholestasis.
Article in Hepatology (Baltimore, Md.), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 57 citations in OpenAlex.
- STAT1/3/5 Functions Driving Lipid and Energy Metabolism in Cancer and Immunity.International journal of molecular sciences · 2026Review
- Metamorphosing macrophages promote placental fibrosis by upregulating the transcription factor STAT5A.Journal of translational medicine · 2026Article
- Role of HNF6 in liver homeostasis and pathophysiology.Molecular medicine (Cambridge, Mass.) · 2025Review
- Liver-specific actions of GH and IGF1 that protect against MASLD.Nature reviews. Endocrinology · 2025 · on this mapReview
- Mechanism and endoscopic-treatment-induced evolution of biliary non-anastomotic stricture after liver transplantation revealed by single-cell RNA sequencing.Clinical and translational medicine · 2024Article
- Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023Review
- Review
- A Mouse Model to Assess STAT3 and STAT5A/B Combined Inhibition in Health and Disease Conditions.Cancers · 2019Article
- Hepatic gene body hypermethylation is a shared epigenetic signature of murine longevity.PLoS genetics · 2018Article
- Validation of insulin-like growth factor-1 as a prognostic parameter in patients with hepatocellular carcinoma in a European cohort.BMC cancer · 2018Article
- Bone marrow derived-mesenchymal stem cells downregulate IL17A dependent IL6/STAT3 signaling pathway in CCl4-induced rat liver fibrosis.PloS one · 2018Article
- The Role of Signal Transducer and Activator of Transcription 5 and Transforming Growth Factor-β1 in Hepatic Fibrosis Induced by Chronic Hepatitis C Virus Infection in Egyptian Patients.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2018Article
- Epidermal growth factor signaling protects from cholestatic liver injury and fibrosis.Journal of molecular medicine (Berlin, Germany) · 2017Article
- DA Negatively Regulates IGF-I Actions Implicated in Cognitive Function via Interaction of PSD95 and nNOS in Minimal Hepatic Encephalopathy.Frontiers in cellular neuroscience · 2017Article
- Review
- Article
- Animal models in primary biliary cirrhosis and primary sclerosing cholangitis.Clinical reviews in allergy & immunology · 2015Review
- Mesenchymal stromal cells engineered to produce IGF-I by recombinant adenovirus ameliorate liver fibrosis in mice.Stem cells and development · 2015Article
- Growth hormone resistance exacerbates cholestasis-induced murine liver fibrosis.Hepatology (Baltimore, Md.) · 2015Article
- Hepatic Hedgehog signaling contributes to the regulation of IGF1 and IGFBP1 serum levels.Cell communication and signaling : CCS · 2014Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
Abstract
unlabelledGrowth hormone (GH) resistance and low serum levels of insulinlike growth factor 1 (IGF-1) are common features in human liver fibrosis and cirrhosis. Signal transducer and activator of transcription 5 (STAT5) controls several vital functions in the liver, including GH-mediated transcription of IGF-1. To investigate the role of STAT5 in liver fibrogenesis, we specifically deleted the Stat5a/b locus both in hepatocytes and cholangiocytes in the multidrug resistance gene 2 knockout (Mdr2(-/-)) mouse model of cholestasis. Double knockout mice develop an early and severe liver fibrosis phenotype, accompanied by perturbed expression of key regulators of bile acid homeostasis. Deletion of Stat5 resulted in GH resistance, and IGF-1 levels in serum were undetectable. We could observe reduced expression of important hepatoprotective genes, such as epidermal growth factor receptor (Egfr), hepatocyte nuclear factor 6 (Hnf6), prolactin receptor (Prlr), and leukemia inhibitory factor receptor (Lifr) as well as increased numbers of apoptotic hepatocytes.
conclusionOur data suggest that loss of STAT5 sensitizes hepatocytes to bile acid-induced damage and apoptosis caused by disruption of GH-induced transcription of Igf-1 and down-regulation of hepatoprotective genes. These findings could contribute to the understanding of liver fibrosis and future treatment strategies for liver fibrosis.
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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.