γ-catenin alleviates cardiac fibrosis through inhibiting phosphorylation of GSK-3β
Xin Tang
Jiaxin Tian
Liping Xie
Yong Ji
1.Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention and Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China2.Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention and Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China3.Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention and Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China4.Key Laboratory of Cardiovascular and Cerebrovascular Medicine, Key Laboratory of Targeted Intervention and Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, Nanjing Medical University, Nanjing, Jiangsu 211166, China
摘要：Cardiac fibrosis is a common pathological change of many cardiovascular diseases.β-catenin has been shown to promote fibrosis.However,the precise role of its homolog γ-catenin in the process of fibrosis remains largely unclear.In this study,we found that the expression of γ-catenin was significantly decreased in angiotensin Ⅱ (Ang Ⅱ)-induced cardiac fibrosis model,contrary to most reports of β-catenin.Overexpression of γ-catenin in cardiac fibroblasts (CFs) significantly inhibited the expression of α-smooth muscle actin (α-SMA),whereas knocking down the expression of γ-catenin with siRNA promoted the occurrence of cardiac fibrosis.Mechanistically,γ-catenin could bind to GSK-3β to inhibit the phosphorylation of GSK-3β,therefore preventing cardiac fibrosis.Our study shows that γ-catenin is an important protective factor in cardiac fibrosis,which provides a new potential target for the treatment of cardiac fibrosis.
机标关键词：
分类号：R542.2(心脏、血管（循环系）疾病)
资助基金：This work was supported by grants from the National Natural Science Foundation of China (Grant No.81670209)
论文发表日期：2020-01-30
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：9( 27-35 )
英文信息