College of Veterinary Medicine, South China Agricultural University, Guangzhou 510642, China.
Faculty of Veterinary and Animal Sciences, The Islamia University of Bahawalpur, 63100, Pakistan.
Biomed Res Int. 2022 Sep 17;2022:6459585. doi: 10.1155/2022/6459585. eCollection 2022.
Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen-containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial-endoplasmic reticulum communication-mediated oxidative stress and autophagy. Mitochondria and endoplasmic reticulum being important organelles in cells are directly or indirectly connected to each other through mitochondria-associated endoplasmic reticulum membranes and jointly regulate oxidative stress and autophagy. The reactive oxygen species (ROS) produced by the mitochondrial respiratory chain are the main inducers of oxidative stress. Damaged mitochondria can be effectively cleared by the process of mitophagy mediated by PINK1/parkin pathway, Nix/BNIP3 pathways, and FUNDC1 pathway, avoiding excessive ROS production. However, the mechanism of mitochondrial-endoplasmic reticulum communication in the regulation of oxidative stress and autophagy is rarely known. For this reason, this review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial-endoplasmic reticulum communication.
氧化应激是自由基和抗氧化系统之间的失衡，导致自由基（含氧分子）过度产生，最终导致脂质过氧化、蛋白质变性和 DNA 突变等氧化损伤。氧化应激可以通过降解受损的细胞器或局部细胞质来激活自噬，以减轻氧化损伤并维持细胞的正常生理活动。当自噬不能消除氧化应激时，它会激活细胞凋亡级联。本综述简要总结了线粒体-内质网通讯介导的氧化应激和自噬。线粒体和内质网作为细胞中的重要细胞器，通过线粒体相关内质网膜直接或间接相互连接，共同调节氧化应激和自噬。线粒体呼吸链产生的活性氧（ROS）是氧化应激的主要诱导剂。受损的线粒体可以通过 PINK1/parkin 途径、Nix/BNIP3 途径和 FUNDC1 途径介导的自噬过程被有效清除，从而避免 ROS 的过度产生。然而，线粒体-内质网通讯在调节氧化应激和自噬中的机制鲜为人知。为此，本综述通过 ROS 和 Ca 探讨了线粒体和内质网在介导氧化应激和自噬中的相互联系，旨在为通过线粒体-内质网通讯介导的自噬来减轻氧化应激提供部分理论基础。
