DACT2 modulates atrial fibrillation through TGF/β and Wnt signaling pathways
Bairu Luo,
Rui Zheng,
Chaoqun Shi,
Deqing Chen,
Xin Jin,
Jian Hou,
Guangtao Xu,
Bo Hu
Affiliations
Bairu Luo
Department of Clinical Pathology, Jiaxing University Master Degree Cultivation Base, Jiaxing Hospital of Traditional Chinese Medicine, Zhejiang Chinese Medical University, Jiaxing, 314001, ZJ, China
Rui Zheng
Department of Clinical Pathology, The 3rd Clinical Medical College Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310053, ZJ, China
Chaoqun Shi
Department of Pathology, Institute of Forensic Science, Jiaxing University, Jiaxing, 314001, ZJ, China
Deqing Chen
Department of Pathology, Institute of Forensic Science, Jiaxing University, Jiaxing, 314001, ZJ, China
Xin Jin
Department of Pathology, Institute of Forensic Science, Jiaxing University, Jiaxing, 314001, ZJ, China
Jian Hou
Department of Cardiology, The Affiliated Panyu Central Hospital of Guangzhou Medical University, Guangzhou, 510080, GD, China
Guangtao Xu
Department of Pathology, Institute of Forensic Science, Jiaxing University, Jiaxing, 314001, ZJ, China
Bo Hu
Department of Clinical Pathology, Jiaxing Hospital of Traditional Chinese Medicine, the 3rd Clinical Medical College Affiliated to Zhejiang Chinese Medical University, Jiaxing, 314001, ZJ, China; Corresponding author.
Atrial fibrillation (AF) is a common cardiac arrhythmia that seriously affects the quality of life of patients. Effective treatment and prevention are important to control the morbidity and mortality of AF. It has been found that cardiac fibrosis promotes the onset and progression of AF. It is now known that transforming growth factor β (TGF-β), an important fibrotic cytokine, plays an important role in cardiac fibrosis by inducing myofibroblast activation via the activation of classical (SMAD-based) and non-classical (non-SMAD-based) signaling pathways. In addition, specific activation of the Wnt/β-catenin pathway has been shown to promote the transformation of fibroblasts into myofibroblasts. In recent years, a new family of proteins, namely Disheveled-associated antagonist of beta-catenin (DACT) 2, can affect the Wnt/β-catenin and TGF-β signaling pathways by regulating the phosphorylation levels of these target proteins, which in turn affects the progression of fibrosis. The present study focuses on the effect of DACT2-guided β-catenin on atrial fibrosis. It is expected that the summarized information can be helpful in the treatment of AF.
