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Article Abstract
Purpose: Cardiovascular diseases, exacerbated by cardiac fibrosis, are the leading causes of mortality. We aimed to determine the role of quercetin (QU) in cardiac fibrosis and the underlying mechanism.
Methods: In this study, 8-week-old mice were subjected to either transverse aortic constriction (TAC) or sham surgery, then they were administered QU or saline. Thereafter, cardiac function and cardiac hypertrophy were accessed. In vitro, cardiac fibroblasts (CFs) were treated with angiotensin II (Ang II) with or without QU. Western blot, qPCR, EdU incorporation assay, and immunofluorescence staining analysis were used to investigate the molecular and cellular features.
Results: For the TAC mouse model, cardiac fibrosis was alleviated by QU. The study revealed that the trans-differentiation and proliferation of CFs promoted by Ang II would be reversed by QU in vitro. Mechanistically, QU exerted the anti-fibrotic effect by regulating the SIRT3/TGF-β/Smad3 signaling pathway.
Conclusion: Quercetin protects against cardiac fibrosis by mediating the SIRT3 signaling pathway.
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