Zhang Junhao, Jin Jinghua, Yang Wei
Institute of Neuroscience, Zhejiang University School of Medicine, Hangzhou 310058, China.
Zhejiang Da Xue Xue Bao Yi Xue Ban. 2019 Jul 25;48(5):552-559. doi: 10.3785/j.issn.1008-9292.2019.10.14.
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（VSMC）是血管壁的主要细胞成分。VSMC功能的变化，包括表型转化和凋亡，在颅内动脉瘤（IA）的发病机制中起关键作用。自噬可通过调节细胞功能参与血管功能的调节。在IA的初始阶段，自噬的激活可加速VSMC的表型转化并抑制VSMC凋亡。随着IA的进展，自噬与凋亡的关系从拮抗转变为协同或促进，大量凋亡的VSMC导致IA破裂。在本综述中，我们描述了自噬在IA发生、发展和破裂过程中调节VSMC功能的作用，以进一步了解IA的发病机制并寻找预防IA形成和破裂的分子靶点。
