Apoptosis Research Centre, School of Natural Sciences, National University of Ireland, Galway, University Road., Galway, Ireland.
Pharmacol Ther. 2012 Jun;134(3):306-16. doi: 10.1016/j.pharmthera.2012.02.003. Epub 2012 Feb 17.
The endoplasmic reticulum (ER) is an elaborate cellular organelle essential for cell function and survival. Conditions that interfere with ER function lead to the accumulation and aggregation of unfolded proteins which are detected by ER transmembrane receptors that initiate the unfolded protein response (UPR) to restore normal ER function. If the ER stress is prolonged, or the adaptive response fails, apoptotic cell death ensues. Many studies have focused on how this failure initiates apoptosis, particularly because ER stress-induced apoptosis is implicated in the pathophysiology of several neurodegenerative and cardiovascular diseases. In this review we aim to shed light on the proteins that are not core components of the UPR signaling pathway but which can influence the course of the ER stress response by regulating the switch from the adaptive phase to apoptosis.
内质网（ER）是一种精细的细胞细胞器，对细胞功能和生存至关重要。干扰 ER 功能的条件会导致未折叠蛋白质的积累和聚集，这些蛋白质被 ER 跨膜受体检测到，从而启动未折叠蛋白反应（UPR）以恢复正常的 ER 功能。如果 ER 应激持续存在，或者适应性反应失败，细胞凋亡就会发生。许多研究都集中在这种失败如何引发细胞凋亡，特别是因为 ER 应激诱导的细胞凋亡与几种神经退行性和心血管疾病的病理生理学有关。在这篇综述中，我们旨在阐明那些不是 UPR 信号通路核心组成部分的蛋白质，这些蛋白质可以通过调节从适应性阶段到细胞凋亡的转变来影响 ER 应激反应的过程。
