ArticleCell cycle (Georgetown, Tex.)2020
MG53/CAV1 regulates transforming growth factor-β1 signaling-induced atrial fibrosis in atrial fibrillation.
Article in Cell cycle (Georgetown, Tex.), 2020. 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.
- Emerging Role and Potential Therapeutic Application of TRIM Proteins in Cardiovascular Diseases.Biomolecules · 2026Review
- Sodium Alginate Hydrogel Infusion of Bone Marrow Mesenchymal Stem Cell-Derived Extracellular Vesicles and p38α Antagonistic Peptides in Myocardial Infarction Fibrosis Mitigation.Journal of the American Heart Association · 2025Article
- CAV1 Protein Encapsulated in Mouse BMSC-Derived Extracellular Vesicles Alleviates Myocardial Fibrosis Following Myocardial Infarction by Blocking the TGF-β1/SMAD2/c-JUN Axis.Journal of cardiovascular translational research · 2024Article
- Gene Polymorphism and Recurrent Atrial Fibrillation after Catheter Ablation: A Comprehensive Review.Reviews in cardiovascular medicine · 2023Review
- MG53: A potential therapeutic target for kidney disease.Pharmacology research & perspectives · 2023Review
- Integrated transcriptomic and proteomic analysis reveals potential targets for heart regeneration.Biomolecules & biomedicine · 2023Article
- Advances in the Study of MG53 in Cardiovascular Disease.International journal of general medicine · 2023Review
- Autophagy in intestinal fibrosis: relevance in inflammatory bowel disease.Frontiers in pharmacology · 2023Review
- Is MG53 a potential therapeutic target for cancer?Frontiers in endocrinology · 2023Review
- The Dose-Dependent Effects of Spironolactone on TGF-Cardiology research and practice · 2021Article
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6 authors.
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Abstract
Atrial fibrosis plays a significant role in the development of atrial fibrillation (AF). Previously, we showed that mitsugumin 53 (MG53) regulates TGF-β1 signaling pathway-induced atrial fibrosis. Recent studies have shown that caveolin-1 (CAV1) is an important anti-fibrosis signaling mediator that inhibits the TGF-β1 signaling pathway. Here, we further study the mechanism underlying the related action of MG53 and CAV1. We demonstrate that CAV1 expression was decreased while MG53 expression was increased in atrial tissue from AF patients. In cultured atrial fibroblasts, MG53 depletion by siRNA caused CAV1 upregulation and TGF-β1/SMAD2 signaling pathway downregulation, while MG53 overexpression via adenovirus had the opposite effect. CAV1 inactivated the TGF-β1/SMAD2 signaling pathway. In addition, using an Ang II-induced fibrosis model, we show that MG53 regulates TGF-β1 signaling via CAV1. Therefore, CAV1 is critical for the MG53 regulation of TGF-β1 signaling pathway-induced atrial fibrosis in AF. These findings reveal the related underlying mechanism of action of MG53 and CAV1 and provide a potential therapeutic target for fibrosis and AF.
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