ArticleNaunyn-Schmiedeberg's archives of pharmacology2019
The dual PPAR-α/γ agonist saroglitazar ameliorates thioacetamide-induced liver fibrosis in rats through regulating leptin.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Cell therapy comparison of dental pulp stem cells, hepatocytes, and their exosomes for liver fibrosis treatment in rats.Animal models and experimental medicine · 2026Article
- Aloe vera gel extract and bone marrow mesenchymal stem cells ameliorate thioacetamide-induced liver fibrosis via modulating lincRNA-p21/miR-17-5p axis.Anatomy & cell biology · 2026Article
- Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- The effect of saraglitazar on TGF-β-induced smad3 phosphorylation and expression of genes related to liver fibrosis in LX2 cell line.Molecular biology reports · 2024Article
- Recent Advances in Research on Active Compounds Against Hepatic Fibrosis.Current medicinal chemistry · 2024Review
- Emerging Role of Nuclear Receptors for the Treatment of NAFLD and NASH.Metabolites · 2022Review
- Leptin Enhances Hepatic Fibrosis and Inflammation in a Mouse Model of Cholestasis.The American journal of pathology · 2022Article
- Mechanistic insights into the peroxisome proliferator-activated receptor alpha as a transcriptional suppressor.Frontiers in medicine · 2022Review
- PPAR Gamma and Viral Infections of the Brain.International journal of molecular sciences · 2021Review
- Parthenolide plays a protective role in the liver of mice with metabolic dysfunction‑associated fatty liver disease through the activation of the HIPPO pathway.Molecular medicine reports · 2021Article
- Regulation of Pancreatic Fibrosis by Acinar Cell-Derived Exosomal miR-130a-3p via Targeting of Stellate Cell PPAR-γ.Journal of inflammation research · 2021Article
- The Agonists of Peroxisome Proliferator-Activated Receptor-γ for Liver Fibrosis.Drug design, development and therapy · 2021Review
- Current and Emerging Approaches for Hepatic Fibrosis Treatment.Gastroenterology research and practice · 2021Review
- Destruction of the stem cell Niche, Pathogenesis and Promising Treatment Targets for Primary Scarring Alopecias.Stem cell reviews and reports · 2020Review
- Review
- Bergenin Attenuates Hepatic Fibrosis by Regulating Autophagy Mediated by the PPAR-PPAR research · 2020Article
- The pharmacodynamic and differential gene expression analysis of PPAR α/δ agonist GFT505 in CDAHFD-induced NASH model.PloS one · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a challenging global health problem resulting from chronic liver injury with no treatment currently available. It has been shown that activators for different peroxisome proliferator-activated receptor (PPAR) isoforms (α, γ, and δ) can affect different pathways in liver fibrosis. To evaluate the effects of the dual PPAR-α/γ agonist saroglitazar (SGZ) against thioacetamide (TAA)-induced fibrosis in rats, SGZ was administered for 6 weeks together with TAA injection. Administration of SGZ ameliorated TAA-induced elevation in hepatic biomarkers. SGZ was able to inhibit periportal and intralobular fibrous connective tissue proliferation, to decrease hydroxyproline content, and to lower alpha smooth muscle actin (α-SMA) protein expression. To unearth the antifibrotic mechanism of SGZ, the role of several fibrotic markers was studied. SGZ possesses inhibitory effect on protein levels of leptin, transforming growth factor-beta 1 (TGF-β1) and platelet-derived growth factor-BB (PDGF-BB). Furthermore, SGZ rectified matrix degradation through decreasing tissue inhibitor of metalloproteinases-1 (TIMP-1). This study suggests that SGZ could have a possible antifibrotic effect via suppression of leptin that can repress TGF-β1 and PDFG-BB, with subsequent inhibition of TIMP-1.
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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.