2. Academic Validation
  3. Daidzein suppresses TGF-β1-induced cardiac fibroblast activation via the TGF-β1/SMAD2/3 signaling pathway

Daidzein suppresses TGF-β1-induced cardiac fibroblast activation via the TGF-β1/SMAD2/3 signaling pathway

  • Eur J Pharmacol. 2022 Mar 15;919:174805. doi: 10.1016/j.ejphar.2022.174805.
Jiangcheng Shu 1,  Lizhi Hu 2,  Yichen Wu 1,  Long Chen 2,  Kai Huang 1,  Zhaohui Wang 3,  Minglu Liang 4
Affiliations

Affiliations

  • 1 Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 2 Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
  • 3 Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: wuxiaohongtian@163.com.
  • 4 Clinic Center of Human Gene Research, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. Electronic address: liangml@hust.edu.cn.
PMID: 35151651 DOI: 10.1016/j.ejphar.2022.174805
Abstract

Myocardial fibrosis is a concomitant bioprocess associated with many cardiovascular diseases (CVDs). Daidzein is an isoflavone that has been used for the treatment of CVDs. This study aimed to reveal its role in myocardial fibrosis. Our results indicate that daidzein had a nontoxic effect on cardiac fibroblasts and that TGF-β1 and TGFβRI levels were gradually decreased by daidzein in a dose-dependent manner. In the current study, we show that daidzein significantly inhibited TGF-β1-induced mRNA and protein expression of α-SMA, collagen I, and collagen III. Accordingly, immunofluorescence staining of α-SMA was performed. Daidzein also inhibited TGF-β1-induced cardiac fibroblast proliferation and migration. Mechanistically, daidzein inhibited the TGF-β/SMAD signaling pathway induced by TGF-β1 in cardiac fibroblasts. Additionally, daidzein ameliorated MI-induced cardiac dysfunction and cardiac fibrosis in vivo. Based on these findings, we conclude that daidzein reduces TGF-β1-induced cardiac fibroblast activation by partially regulating the TGF-β1/SMAD2/3 signaling pathway.

Keywords

Cardiac fibroblasts; Daidzein; Myocardial fibrosis; TGF-β1; TGF-β1/SMAD2/3 signaling pathway.

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