纤维化引起心房电传导功能障碍导致心房颤动的机制及其抗纤维化治疗

Mechanism of Atrial Fibrillation Caused by Electrical Conduction Dysfunction after Atrial Fibrosis and Its AntiFibrosis Treatment

心房纤维化可导致心房电传导速度减慢,传导方向异质性,引起并维持心房颤动的发生。肌成纤维细胞(MFbs)是心肌纤维化的主要作用细胞,其通过转化生长因子β1、结缔组织生长因子、血小板衍生生长因子、基质金属蛋白酶以及金属蛋白酶组织抑制因子等多种细胞因子和酶作用促进心肌纤维化。而MFbs迁移至损伤区域引起的胶原蛋白沉积、缝隙连接蛋白表达异常以及释放旁分泌因子影响心肌电传导功能。在基础疾病早期干预,抑制心房纤维化,改善心房电传导功能,有望成为防治心房颤动的新型手段。

Atrial fibrosis can lead to slow electrical conduction velocity, induce conduction direction heterogeneity, which can cause and maintain the occurrence of atrial fibrillation. Myofibroblasts （MFbs） are the major effeetor cells of myocardial fibrosis. MFbs promote cardiac fibrosis by transforming growth factor-151 , connective tissue growth factor, plateletderived growth factor, matrix metalloproteinases, tissue inhibitor of metalloproteinases and other cytokines and enzymes. MFbs migrate to the injured areas and proliferate rapidly, causing collagen deposition, abnormal connexin expression and release of paracrine factors that can affect electrical conduction. Early intervention in the underlying disease--inhibition of atrial fibrosis and improvement of atrial conduction function,is expected to become a new prevention and treatment of atrial fibrillation.