内质网
未折叠蛋白反应
内皮功能障碍
内皮
平衡
细胞生物学
炎症
氧化应激
生物
调节器
内皮干细胞
发病机制
免疫学
内分泌学
生物化学
基因
体外
作者
Micah L. Battson,Dustin M. Lee,Christopher L. Gentile
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physiological Society]
日期:2017-03-01
卷期号:312 (3): H355-H367
被引量:77
标识
DOI:10.1152/ajpheart.00437.2016
摘要
The vascular endothelium plays a critical role in cardiovascular homeostasis, and thus identifying the underlying causes of endothelial dysfunction has important clinical implications. In this regard, the endoplasmic reticulum (ER) has recently emerged as an important regulator of metabolic processes. Dysfunction within the ER, broadly termed ER stress, evokes the unfolded protein response (UPR), an adaptive pathway that aims to restore ER homeostasis. Although the UPR is the first line of defense against ER stress, chronic activation of the UPR leads to cell dysfunction and death and has recently been implicated in the pathogenesis of endothelial dysfunction. Numerous risk factors for endothelial dysfunction can induce ER stress, which may in turn disrupt endothelial function via direct effects on endothelium-derived vasoactive substances or by activating other pathogenic cellular networks such as inflammation and oxidative stress. This review summarizes the available data linking ER stress to endothelial dysfunction.
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