Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Department of Cardiovascular Medicine, the Second Affiliated Hospital of Nanchang University, Nanchang 330006, China.
Eur J Pharmacol. 2018 Oct 15;837:1-7. doi: 10.1016/j.ejphar.2018.08.030. Epub 2018 Aug 25.
The pathogenesis of atrial fibrillation (AF) is largely dependent on structural remodeling and electrical reconfiguration, which in turn drive localized fibrosis. Canonical transient receptor potential 3 (TRPC3) channel is indispensable regulator of fibrosis development, promoting fibroblasts to transition into myofibroblasts via intracellular Ca overload. TRPC3 is a non-voltage gated, non-selective cation channel that regulates the permeability of the cell to Ca. When subjected to various external physical and chemical stimuli, such as angiotensin II (AngII), mechanical stretch, hypoxia, or oxidative stress, TRPC3 coordinates with downstream signal transduction pathways to alter gene expression and thereby regulate a number of distinct pathological patterns and mechanisms. This review will focus on how TRPC3 affects AF pathogenesis by exploring the underlying mechanisms governing fibrosis associated with particular signaling proteins, ultimately highlighting the characteristics of TPRC3 that mark it as a novel therapeutic target for AF alleviation.
心房颤动（AF）的发病机制在很大程度上依赖于结构重塑和电重构，而这反过来又会导致局部纤维化。经典瞬时受体电位 3（TRPC3）通道是纤维化发展不可缺少的调节剂，通过细胞内 Ca 超载促进成纤维细胞向肌成纤维细胞转化。TRPC3 是一种非电压门控、非选择性阳离子通道，调节细胞对 Ca 的通透性。当受到血管紧张素 II（AngII）、机械拉伸、缺氧或氧化应激等各种外部物理和化学刺激时，TRPC3 与下游信号转导途径协调，改变基因表达，从而调节许多不同的病理模式和机制。本综述将重点探讨 TRPC3 通过探索与特定信号蛋白相关的纤维化相关的潜在机制如何影响 AF 的发病机制，最终突出 TPRC3 的特征，将其标记为治疗 AF 的新型靶点。
