血管纤维化的分子机制及研究进展

Molecular mechanism and research progress of vascular fibrosis

摘要:

血管纤维化是心血管疾病进展的核心病理过程,其特征为血管壁中细胞外基质(ECM)的异常沉积与重塑,最终导致血管弹性丧失、血流动力学紊乱及终末器官损伤。该过程涉及血管平滑肌细胞(VSMC)表型转化、内皮-间质转化(EndMT)及炎症纤维化网络激活,其机制包括多细胞交互、信号通路串扰及表观遗传调控。本文系统综述了血管纤维化的病理生理基础、关键的分子及信号网络,结合当前研究现状,探讨了潜在治疗靶点与临床转化挑战,并对未来发展方向进行了展望。

Abstract:

Vascular fibrosis is the core pathological process of cardiovascular disease progression, which is characterized by abnormal deposition and remodeling of extracellular matrix (ECM) in the vascular wall. This results in the loss of vascular elasticity, hemodynamic derangement, and end-organ damage. This process involves the phenotypic transformation of vascular smooth muscle cell (VSMC), endothelial-mesenchymal transition (EndMT), and activation of inflammatory-fibrotic networks. The mechanisms include multicellular interactions, signaling pathway crosstalk, and epigenetic regulation. This article systematically reviews the pathophysiological basis, key molecules and signaling networks of vascular fibrosis, discusses potential therapeutic targets and clinical translation challenges based on current research status, and provides an outlook on future development directions.