DACT2 modulates atrial fibrillation through TGF/(3 and Wnt signaling pathways

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 (3 (TGF-(3), 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/(3-catenin pathway has been shown to promote the transformation of fibroblasts into myofibroblasts. In recent years, a new family of proteins, namely Disheveledassociated antagonist of beta-catenin (DACT) 2, can affect the Wnt/(3-catenin and TGF-(3 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 (3-catenin on atrial fibrosis. It is expected that the summarized information can be helpful in the treatment of AF.