ArticleJournal of physiology and biochemistry2021
Regulation of peroxisome proliferator-activated receptor-gamma activity affects the hepatic stellate cell activation and the progression of NASH via TGF-β1/Smad signaling pathway.
Article in Journal of physiology and biochemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 41 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- Pioglitazone protects against thioacetamide-induced liver fibrosis via AMPK-mediated inhibition of the TGF-β/Smad fibrotic cascade.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Cell therapy comparison of dental pulp stem cells, hepatocytes, and their exosomes for liver fibrosis treatment in rats.Animal models and experimental medicine · 2026Article
- Platelet-mediated progression of fatty liver disease in metabolic dysfunction-associated steatohepatitis: a pathophysiological review.Frontiers in medicine · 2026Review
- ETS1 suppresses hepatic stellate cell activation and liver fibrosis.JCI insight · 2025Article
- NUP85 siRNA loaded red blood cell-derived extracellular vesicles alleviate hepatic steatosis in MASLD.Journal of nanobiotechnology · 2025Article
- MASLD development: From molecular pathogenesis toward therapeutic strategies.Chinese medical journal · 2025Review
- Thymoquinone mitigates cardiac hypertrophy by activating adaptive autophagy via the PPAR‑γ/14‑3‑3γ pathway.International journal of molecular medicine · 2025Article
- Reduction of Low-Density Lipoprotein Cholesterol by Mesenchymal Stem Cells in a Mouse Model of Exogenous Cushing's Syndrome.Tissue engineering and regenerative medicine · 2025Article
- Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Artemether Attenuates High Glucose-Induced Inflammation and Fibrogenesis in Renal Tubular Epithelial Cells by Modulating the TGF-Journal of diabetes research · 2025Article
- Non-targeted metabolomics and network pharmacology of Taohong Siwu Decoction in hepatic fibrosis mouse model using high resolution mass spectrometry.Frontiers in molecular biosciences · 2025Article
- Nephroprotective effect of pioglitazone in a Wistar rat model of adenine‑induced chronic kidney disease.Experimental and therapeutic medicine · 2024Article
- Application of PPAR Ligands and Nanoparticle Technology in Metabolic Steatohepatitis Treatment.Biomedicines · 2024Review
- Article
- Targeting nuclear receptors for NASH/MASH: From bench to bedside.Liver research (Beijing, China) · 2024Article
- Epigenetic modification in liver fibrosis: Promising therapeutic direction with significant challenges ahead.Acta pharmaceutica Sinica. B · 2024Review
- Recent Advances in Research on Active Compounds Against Hepatic Fibrosis.Current medicinal chemistry · 2024Review
- Reduction in Obesity-Related Hepatic Fibrosis by SR1664.Biology · 2023Article
- Recent progress in molecular mechanisms of postoperative recurrence and metastasis of hepatocellular carcinoma.World journal of gastroenterology · 2022Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Development of liver fibrosis is associated with activation of quiescent hepatic stellate cells (HSCs) into myofibroblasts (activated HSCs), which produce excessive extracellular matrix. Peroxisome proliferator-activated receptor-gamma (PPAR-γ) exerts protective effects on hepatic inflammation and fibrosis. The current study was to explore the function of PPAR-γ on HSC activation and progression of nonalcoholic steatohepatitis (NASH). Our study found that HSCs were gradually activated during the progression of methionine-choline-deficient (MCD) diet-induced NASH, accompanied by decreased PPAR-γ expression and activated TGF-β1/Smad signaling pathway in the liver. PPAR-γ agonist was found to inhibit primary HSCs and NIH/3T3 fibroblast activation and reverted their phenotypical morphology induced by TGF-β1 in vitro. In addition to this, PPAR-γ agonist decreased expression of TGF-β1 and phosphorylation of Smad2/3 while increased expression of Smad7. In vivo, rosiglitazone, a PPAR-γ agonist, inhibited HSC activation and alleviated liver fibrosis and inflammation similarly via inhibiting the activation of TGF-β1/Smad signaling pathway. In parallel, rosiglitazone alleviated hepatic lipid accumulation and peroxidation, beneficial to reverse of NASH. From these findings, it can be concluded that the gradual activation of HSCs is crucial to the progression of NASH and modulating PPAR-γ expression can affect HSC activation via TGF-β1/Smad signaling pathway and thereby influence hepatic fibrogenesis.
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