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内质网-线粒体界面的凋亡信号。

Apoptotic signals at the endoplasmic reticulum-mitochondria interface.

机构信息

Department of Biomedical Sciences, University of Padova, Padova, Italy.

Department of Biomedical Sciences, University of Padova, Padova, Italy.

出版信息

Adv Protein Chem Struct Biol. 2021;126:307-343. doi: 10.1016/bs.apcsb.2021.02.007. Epub 2021 Mar 24.

Abstract

The maintenance of cellular homeostasis involves the participation of multiple organelles, such as the endoplasmic reticulum (ER) and mitochondria. Specifically, ER plays a key role in calcium (Ca) storage, lipid synthesis, protein folding, and assembly, while mitochondria are the "energy factories" and provide energy to drive intracellular processes. Hence, alteration in ER or mitochondrial homeostasis has detrimental effects on cell survival, being linked to the triggering of apoptosis, a programmed form of cell death. Besides, ER stress conditions affect mitochondria functionality and vice-versa, as ER and mitochondria communicate via mitochondria-associated ER membranes (MAMs) to carry out a number of fundamental cellular functions. It is not surprising, thus, that also MAMs perturbations are involved in the regulation of apoptosis. This chapter intends to accurately discuss the involvement of MAMs in apoptosis, highlighting their crucial role in controlling this delicate cellular process.

摘要

细胞内环境稳态的维持涉及多个细胞器的参与,如内质网(ER)和线粒体。具体来说,ER 在钙(Ca)储存、脂质合成、蛋白质折叠和组装中发挥关键作用,而线粒体则是“能量工厂”,为驱动细胞内过程提供能量。因此,内质网或线粒体内环境稳态的改变对细胞存活有不利影响,与凋亡的触发有关,凋亡是一种程序性细胞死亡形式。此外,内质网应激条件会影响线粒体的功能,反之亦然,因为内质网和线粒体通过线粒体相关内质网膜(MAMs)进行通讯,以执行许多基本的细胞功能。因此,MAMs 的扰动也参与了凋亡的调节也就不足为奇了。本章旨在准确讨论 MAMs 在凋亡中的作用,强调它们在控制这一微妙细胞过程中的关键作用。

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