ArticleScientific reports2020
Ghrelin reverses ductular reaction and hepatic fibrosis in a rodent model of cholestasis.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Senkyunolide A ameliorates cholestatic liver fibrosis by controlling CLCC1-mediated endoplasmic reticulum CaActa pharmacologica Sinica · 2025Article
- Exploring the Antifibrotic Mechanisms of Ghrelin: Modulating TGF-β Signalling in Organ Fibrosis.Expert reviews in molecular medicine · 2024Review
- Molecular and cellular mechanisms underlying the hepatoprotective role of ghrelin against NAFLD progression.Journal of physiology and biochemistry · 2023Review
- Ghrelin regulating liver activity and its potential effects on liver fibrosis andFrontiers in cellular and infection microbiology · 2023Review
- Leptin Enhances Hepatic Fibrosis and Inflammation in a Mouse Model of Cholestasis.The American journal of pathology · 2022Article
- Predictive and Diagnostic Value of Serum Adipokines in Pregnant Women with Intrahepatic Cholestasis.International journal of environmental research and public health · 2022Article
- Enteroendocrine Cell Formation Is an Early Event in Pancreatic Tumorigenesis.Frontiers in physiology · 2022Article
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
Abstract
The orexigenic peptide ghrelin (Ghr) stimulates hunger signals in the hypothalamus via growth hormone secretagogue receptor (GHS-R1a). Gastric Ghr is synthetized as a preprohormone which is proteolytically cleaved, and acylated by a membrane-bound acyl transferase (MBOAT). Circulating Ghr is reduced in cholestatic injuries, however Ghr's role in cholestasis is poorly understood. We investigated Ghr's effects on biliary hyperplasia and hepatic fibrosis in Mdr2-knockout (Mdr2KO) mice, a recognized model of cholestasis. Serum, stomach and liver were collected from Mdr2KO and FVBN control mice treated with Ghr, des-octanoyl-ghrelin (DG) or vehicle. Mdr2KO mice had lower expression of Ghr and MBOAT in the stomach, and lower levels of circulating Ghr compared to WT-controls. Treatment of Mdr2KO mice with Ghr improved plasma transaminases, reduced biliary and fibrosis markers. In the liver, GHS-R1a mRNA was expressed predominantly in cholangiocytes. Ghr but not DG, decreased cell proliferation via AMPK activation in cholangiocytes in vitro. AMPK inhibitors prevented Ghr-induced FOXO1 nuclear translocation and negative regulation of cell proliferation. Ghr treatment reduced ductular reaction and hepatic fibrosis in Mdr2KO mice, regulating cholangiocyte proliferation via GHS-R1a, a G-protein coupled receptor which causes increased intracellular Ca
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