自噬
血管平滑肌
细胞生物学
医学
细胞内
细胞外基质
再狭窄
程序性细胞死亡
生物
平滑肌
内科学
细胞凋亡
生物化学
支架
作者
Shi Tai,Xinqun Hu,Daoquan Peng,Shenghua Zhou,Xi-Long Zheng
标识
DOI:10.1016/j.ijcard.2016.02.128
摘要
Autophagy, which is an evolutionarily conserved mechanism and links to several cellular pathways, impacts vascular smooth muscle cells (VSMCs) survival and function. Activation of autophagy by intercellular and/or extracellular stimuli has protective effects on VSMCs against cell death, while on the contrary, overloading autophagy has been recognized as a deleterious process by excessive self-digestion. Alterations in autophagy has been documented in VSMC in response to various stimuli, resulting in modulation of VSMC functions, including proliferation, migration, matrix secretion, contraction/relaxation, and differentiation. Each of these changes in VSMC functions plays a critical role in the development of vascular diseases. Importantly, emerging evidence demonstrates that autophagy deficiency in VSMCs would contribute to atherosclerosis and restenosis, shedding novel light on therapeutic target of the vascular disorders. Herein, this review summarizes the recent progress associated with the roles of autophagy in VSMC and offers the perspectives to several challenges and future directions for further studies.
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