关键词: ER stress Endoplasmic reticulum Hypoxia MERCs Mitochondrial UPR

Mesh : Endoplasmic Reticulum / metabolism Humans Animals Endoplasmic Reticulum Stress / physiology Unfolded Protein Response / physiology Hypoxia / metabolism Apoptosis / physiology Cell Hypoxia / physiology Endoplasmic Reticulum-Associated Degradation

来  源:   DOI:10.1016/j.biopha.2024.116812

Abstract:
The endoplasmic reticulum (ER) is important to cells because of its essential functions, including synthesizing three major nutrients and ion transport. When cellular homeostasis is disrupted, ER quality control (ERQC) system is activated effectively to remove misfolded and unfolded proteins through ER-phagy, ER-related degradation (ERAD), and molecular chaperones. When unfolded protein response (UPR) and ER stress are activated, the cell may be suffering a huge blow, and the most probable consequence is apoptosis. The membrane contact points between the ER and sub-organelles contribute to communication between the organelles. The decrease in oxygen concentration affects the morphology and structure of the ER, thereby affecting its function and further disrupting the stable state of cells, leading to the occurrence of disease. In this study, we describe the functions of ER-, ERQC-, and ER-related membrane contact points and their changes under hypoxia, which will help us further understand ER and treat ER-related diseases.
摘要:
内质网(ER)是重要的细胞,因为它的基本功能,包括合成三种主要营养素和离子运输。当细胞稳态被破坏时,ER质量控制(ERQC)系统被有效激活,通过ER-phagy去除错误折叠和未折叠的蛋白质,ER相关降解(ERAD),和分子伴侣。当未折叠蛋白反应(UPR)和内质网应激被激活时,细胞可能正在遭受巨大的打击,最可能的后果是细胞凋亡.ER和亚细胞器之间的膜接触点有助于细胞器之间的连通。氧浓度的降低影响ER的形态和结构,从而影响其功能并进一步破坏细胞的稳定状态,导致疾病的发生。在这项研究中,我们描述了ER-的功能,ERQC-,和ER相关的膜接触点及其在缺氧条件下的变化,这将有助于我们进一步了解ER和治疗ER相关疾病。
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