ArticleMolecular medicine (Cambridge, Mass.)2012
p38 mitogen-activated protein kinase and liver X receptor-α mediate the leptin effect on sterol regulatory element binding protein-1c expression in hepatic stellate cells.
Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- A novel combination therapy with Uridine and Praziquantel effectively alleviates schistosomiasis-induced hepatic fibrosis through promoting adipogenic differentiation.PLoS pathogens · 2025Article
- Metabolic Sparks in the Liver: Metabolic and Epigenetic Reprogramming in Hepatic Stellate Cells Activation and Its Implications for Human Metabolic Diseases.Diabetes & metabolism journal · 2025Review
- Evaluating the Potential ofPharmaceuticals (Basel, Switzerland) · 2023Review
- Effects of a Combination of Empagliflozin Plus Metformin vs. Metformin Monotherapy on NAFLD Progression in Type 2 Diabetes: The IMAGIN Pilot Study.Biomedicines · 2023Article
- Detangling the interrelations between MAFLD, insulin resistance, and key hormones.Hormones (Athens, Greece) · 2022Review
- Hepatic Stellate Cell Activation and Inactivation in NASH-Fibrosis-Roles as Putative Treatment Targets?Biomedicines · 2021Review
- The Power of Plasticity-Metabolic Regulation of Hepatic Stellate Cells.Cell metabolism · 2021Review
- Role of Leptin in the Digestive System.Frontiers in pharmacology · 2021Review
- Role of cytoglobin, a novel radical scavenger, in stellate cell activation and hepatic fibrosis.Clinical and molecular hepatology · 2020Review
- Review
- Hepatic stellate cells as key target in liver fibrosis.Advanced drug delivery reviews · 2017Review
- GATA binding protein 3 is correlated with leptin regulation of PPARγ1 in hepatic stellate cells.Journal of cellular and molecular medicine · 2017Article
- Pirfenidone controls the feedback loop of the AT1R/p38 MAPK/renin-angiotensin system axis by regulating liver X receptor-α in myocardial infarction-induced cardiac fibrosis.Scientific reports · 2017Article
- Article
- Adipocytokines and hepatic fibrosis.Trends in endocrinology and metabolism: TEM · 2015Review
- Potent natural products and herbal medicines for treating liver fibrosis.Chinese medicine · 2015Article
- Article
- Leptin's role in lipodystrophic and nonlipodystrophic insulin-resistant and diabetic individuals.Endocrine reviews · 2013Review
- The β-catenin pathway contributes to the effects of leptin on SREBP-1c expression in rat hepatic stellate cells and liver fibrosis.British journal of pharmacology · 2013Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leptin, a key hormone in regulating energy homeostasis, is mainly produced by adipocytes. Cogent evidence indicates a unique role of leptin in the promotion of liver fibrosis. Hepatic stellate cell (HSC) activation is a pivotal step in the process of liver fibrosis. Sterol regulatory element binding protein (SREBP)-1c, a critical transcription factor for lipid synthesis and adipocyte differentiation, functions as a key transcription factor in inhibition of HSC activation. SREBP-1c is highly expressed in quiescent HSCs and downregulated upon HSC activation. The aim of this study is to examine the effect of leptin on SREBP-1c gene expression in HSCs in vitro and in vivo and elucidate the underlying mechanisms. The results of the present study demonstrated that leptin strongly inhibited SREBP-1c expression in HSCs in vivo and in vitro. p38 MAPK was involved in leptin regulation of SREBP-1c expression in cultured HSCs. Leptin-induced activation of p38 MAPK led to the decreases in liver X receptor (LXR)-α protein level, activity and its binding to the SREBP-1c promoter, which caused the downregulation of SREBP-1c expression. Moreover, leptin inhibition of SREBP-1c expression via p38 MAPK increased the expression of alpha1(I) collagen in HSCs. Our results might provide new insights into the mechanisms of the unique role of leptin in the development of liver fibrosis and might have potential implications for clarifying the molecular mechanisms underlying liver fibrosis in diseases in which circulating leptin levels are elevated such as nonalcoholic steatohepatitis, type 2 diabetes mellitus and alcoholic cirrhosis.
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