心房颤动相关心肌纤维化的信号通路研究进展

Research progress on signaling pathways underlying myocardial fibrosis in atrial fibrillation

摘要:

心肌纤维化是心房颤动发生与发展的重要病理基础，发生机制涉及多种信号通路，其中存在多种信号通路共同作用，或与炎症反应相互作用。经典信号通路如TGF-β/Smad通路、Wnt/β-catenin通路激活成纤维细胞增殖、上调纤维化相关蛋白表达。PI3K/Akt通路、NF-κB信号通路除了直接激活成纤维细胞外，还增强了炎症因子表达，间接促进心肌纤维化和心房重塑发生。还有一些小众的信号通路也在心房颤动、心肌纤维化的发展中发挥着重要作用。上述信号通路不仅直接促进心肌纤维化，还通过复杂的分子交互调控其进程，对这些通路的深入研究将为心肌纤维化的干预与治疗提供重要理论依据。

Abstract:

Myocardial fibrosis is a critical pathological basis for the onset and progression of atrial fibrillation, involving multiple signaling pathways. These pathways often interact or act synergistically with inflammatory responses. Classical pathways, such as the TGF-β/Smad pathway and the Wnt/β-catenin pathway, promote fibroblast proliferation and upregulate the expression of fibrosis-related proteins. The PI3K/Akt signaling pathway and the NF-κB signaling pathway not only directly activate fibroblasts but also enhance the expression of inflammatory factors, indirectly contributing to myocardial fibrosis and atrial remodeling. Additionally, some less-studied signaling pathways also play significant roles in the progression of myocardial fibrosis in atrial fibrillation. These pathways not only directly drive myocardial fibrosis but also regulate the progression of fibrosis through complex molecular interactions. In-depth research into these signaling pathways will provide valuable theoretical insights for intervention and treatment of atrial myocardial fibrosis.