Highlights the role of collagen dysregulation, MMP/TIMP imbalance, and the TGF-beta1-Smad pathway in the development of atrial fibrosis and maintenance of atrial fibrillation.
Atrial fibrosis in AF is characterized by severe alterations in collagen I and III synthesis/degradation associated with disturbed MMP/TIMP systems and increased levels of RECK. TGF-beta1 contributes to atrial fibrosis via TGF-beta1-Smad pathway by phosphorylating Smad2. These processes culminate in accumulations of fibrillar and non-fibrillar collagens leading to excessive atrial fibrosis and maintainance of AF.
Polyakova et al. (Tue,) studied this question.