Mei Yu, Thompson Melissa D, Cohen Richard A, Tong Xiaoyong
Vascular Biology Section, Boston University School of Medicine, Boston, Massachusetts 02118, USA.
J Pharmacol Biomed Anal. 2013 Nov 15;1(2):1000107.
The endoplasmic reticulum (ER) plays a pivotal role in lipid and protein biosynthesis as well as calcium store regulation, which determines its essential role in cell function. Hypoxia, nutrient deprivation, perturbation of redox status and aberrant calcium regulation can all trigger the ER stress response, which is mediated through three main sensors, namely inositol requiring element-1 (IRE-1), protein kinase-like ER kinase (PERK) and activating transcription factor 6 (ATF6). This review explores the interaction of ER stress and ER stress-associated pathological processes, including inflammation, apoptosis, aberrant autophagy, mitochondrial dysfunction and hypoxic responses. In addition, the correlation of ER stress with lipid and calcium homeostasis and dysregulation, and its role in disease development is also presented. Improved understanding of ER stress and its cofactors in pathological processes may provide new perspective on disease development and control.
内质网（ER）在脂质和蛋白质生物合成以及钙储存调节中起着关键作用，这决定了它在细胞功能中的重要作用。缺氧、营养剥夺、氧化还原状态的扰动和异常的钙调节都可以触发内质网应激反应，该反应由三个主要传感器介导，即肌醇需求酶1（IRE-1）、蛋白激酶样内质网激酶（PERK）和活化转录因子6（ATF6）。本综述探讨了内质网应激与内质网应激相关病理过程的相互作用，包括炎症、凋亡、异常自噬、线粒体功能障碍和缺氧反应。此外，还介绍了内质网应激与脂质和钙稳态及失调的相关性，以及它在疾病发展中的作用。对内质网应激及其在病理过程中的辅助因子的深入了解可能为疾病发展和控制提供新的视角。
