Vascular smooth muscle cells (VSMC) are the main cellular component of vessel wall. The changes of VSMC functions including phenotypic transformation and apoptosis play a critical role in the pathogenesis of intracranial aneurysm (IA). Autophagy can participate in the regulation of vascular function by regulating cell function. In the initial stage of IA, the activation of autophagy can accelerate the phenotypic transformation of VSMC and inhibit VSMC apoptosis. With the progress of IA, the relationship between autophagy and apoptosis changes from antagonism to synergy or promotion, and a large number of apoptotic VSMC lead to the rupture of IA. In this review, we describe the role of autophagy regulating the function of VSMC in the occurrence, development and rupture of IA, for further understanding the pathogenesis of IA and finding molecular targets to prevent the formation and rupture of IA.
血管平滑肌细胞作为血管壁的主要细胞成分，其功能（表型转化、凋亡等）调节在颅内动脉瘤发病中发挥了重要作用。自噬可通过参与细胞功能调控进而参与血管功能的调节。在颅内动脉瘤起始阶段，自噬的激活促使血管平滑肌细胞发生表型转化，并抑制其凋亡；随着颅内动脉瘤的发展，自噬的激活与细胞凋亡由最先的对抗关系转化为协同或推动关系，血管平滑肌细胞大量凋亡导致颅内动脉瘤破裂。本文对自噬调控血管平滑肌细胞功能在颅内动脉瘤发生、发展以及破裂过程中的作用进行了系统阐述，以期为深入理解颅内动脉瘤的发病机制及寻找阻止颅内动脉瘤形成和破裂的分子靶点提供理论基础。