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首页> 外文期刊>The FEBS journal >Cell death induced by endoplasmic reticulum stress
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Cell death induced by endoplasmic reticulum stress

机译：内质网应激诱导的细胞死亡

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摘要

The endoplasmic reticulum is an organelle with multiple functions. The synthesis of transmembrane proteins and proteins that are to be secreted occurs in this organelle. Many conditions that impose stress on cells, including hypoxia, starvation, infections and changes in secretory needs, challenge the folding capacity of the cell and promote endoplasmic reticulum stress. The cellular response involves the activation of sensors that transduce signaling cascades with the aim of restoring homeostasis. This is known as the unfolded protein response, which also intersects with the integrated stress response that reduces protein synthesis through inactivation of the initiation factor eIF2 alpha. Central to the unfolded protein response are the sensors PERK, IRE1 and ATF6, as well as other signaling nodes such as c-Jun N-terminal kinase 1 (JNK) and the downstream transcription factors XBP1, ATF4 and CHOP. These proteins aim to restore homeostasis, but they can also induce cell death, which has been shown to occur by necroptosis and, more commonly, through the regulation of Bcl-2 family proteins (Bim, Noxa and Puma) that leads to mitochondrial apoptosis. In addition, endoplasmic reticulum stress and proteotoxic stress have been shown to induce TRAIL receptors and activation of caspase-8. Endoplasmic reticulum stress is a common feature in the pathology of numerous diseases because it plays a role in neurodegeneration, stroke, cancer, metabolic diseases and inflammation. Understanding how cells react to endoplasmic reticulum stress can accelerate discovery of drugs against these diseases.
机译：内质网是具有多种功能的细胞器。跨膜蛋白和要分泌的蛋白的合成发生在该细胞器中。向细胞施加压力的许多条件，包括缺氧，饥饿，感染和分泌需求的变化，都会挑战细胞的折叠能力并促进内质网应激。细胞应答涉及激活信号传导级联的传感器的恢复，目的是恢复体内平衡。这被称为未折叠的蛋白质反应，也与整合的应激反应相交，后者通过使起始因子eIF2α失活而减少了蛋白质的合成。展开的蛋白质反应的中心是传感器PERK，IRE1和ATF6，以及其他信号节点，例如c-Jun N端激酶1（JNK）和下游转录因子XBP1，ATF4和CHOP。这些蛋白质旨在恢复体内平衡，但它们也可以诱导细胞死亡，这已经显示出是死于尸检，更常见的是通过调节Bcl-2家族蛋白（Bim，Noxa和Puma）导致线粒体凋亡。此外，内质网应激和蛋白毒性应激已显示出诱导TRAIL受体和激活caspase-8的作用。内质网应激是许多疾病病理中的共同特征，因为它在神经变性，中风，癌症，代谢性疾病和炎症中起作用。了解细胞对内质网应激反应的方式可以加速发现针对这些疾病的药物。

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