ArticleCell death & disease2023
The chromatin remodeling protein BRG1 regulates HSC-myofibroblast differentiation and liver fibrosis.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- The Role of Epigenetics in Corneal Fibrosis.Epigenomes · 2026Review
- Identification of GPX3 as a key biomarker of placental ferroptosis in gestational diabetes mellitus via bioinformatics and clinical analysis.Molecular diversity · 2026Article
- Insulin-like growth factor binding proteins in metabolic dysfunction-associated steatotic liver disease.Frontiers in endocrinology · 2026Review
- BRG1 exacerbates myocardial fibrosis after myocardial infarction by interacting with ZEB1.Frontiers in pharmacology · 2026Article
- Recent Advances in the Study of Traditional Chinese Medicine in Reversing Hepatic Fibrosis Through the Regulation of Hepatic Stellate Cells Apoptosis Pathways.Drug design, development and therapy · 2026Review
- SWI/SNF Chromatin Remodelling Complex in Hepatic Physiology: Mechanistic Insights Into Development, Homeostasis and Pathogenesis.Journal of cellular and molecular medicine · 2026Review
- Article
- Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025Review
- Expression of insulin-like growth factor binding protein 5 in the vaginal wall tissues of older women with pelvic organ prolapse.Scientific reports · 2024Article
- Treatment of Thoracic SMARCA4-Deficient Undifferentiated Tumors: Where We Are and Where We Will Go.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive fibrogenic response in the liver disrupts normal hepatic anatomy and function heralding such end-stage liver diseases as hepatocellular carcinoma and cirrhosis. Myofibroblasts, derived primarily from hepatic stellate cells (HSCs), are the effector of liver fibrosis. In the present study we investigated the mechanism by which Brahma-related gene 1 (BRG1, encoded by Smarca4) regulates HSC-myofibroblast transition and the implication in intervention against liver fibrosis. We report that BRG1 expression was elevated during HSC maturation in cell culture, in animal models, and in human cirrhotic liver biopsy specimens. HSC-specific deletion of BRG1 attenuated liver fibrosis in several different animal models. In addition, BRG1 ablation in myofibroblasts ameliorated liver fibrosis. RNA-seq identified IGFBP5 as a novel target for BRG1. Over-expression of IGFBP5 partially rescued the deficiency in myofibroblast activation when BRG1 was depleted. On the contrary, IGFBP5 knockdown suppressed HSC-myofibroblast transition in vitro and mollified liver fibrosis in mice. Mechanistically, IGFBP5 interacted with Bat3 to stabilize the Bat3-TβR complex and sustain TGF-β signaling. In conclusion, our data provide compelling evidence that BRG1 is a pivotal regulator of liver fibrosis by programming HSC-myofibroblast transition.
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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.