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Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy

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 autopha...

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Autores principales: Liu, Xiaoqing, Hussain, Riaz, Mehmood, Khalid, Tang, Zhaoxin, Zhang, Hui, Li, Ying
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9509228/
https://www.ncbi.nlm.nih.gov/pubmed/36164446
http://dx.doi.org/10.1155/2022/6459585
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author Liu, Xiaoqing
Hussain, Riaz
Mehmood, Khalid
Tang, Zhaoxin
Zhang, Hui
Li, Ying
author_facet Liu, Xiaoqing
Hussain, Riaz
Mehmood, Khalid
Tang, Zhaoxin
Zhang, Hui
Li, Ying
author_sort Liu, Xiaoqing
collection PubMed
description 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(2+) and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial-endoplasmic reticulum communication.
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spelling pubmed-95092282022-09-25 Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy Liu, Xiaoqing Hussain, Riaz Mehmood, Khalid Tang, Zhaoxin Zhang, Hui Li, Ying Biomed Res Int Review Article 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(2+) and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial-endoplasmic reticulum communication. Hindawi 2022-09-17 /pmc/articles/PMC9509228/ /pubmed/36164446 http://dx.doi.org/10.1155/2022/6459585 Text en Copyright © 2022 Xiaoqing Liu et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Liu, Xiaoqing
Hussain, Riaz
Mehmood, Khalid
Tang, Zhaoxin
Zhang, Hui
Li, Ying
Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title_full Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title_fullStr Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title_full_unstemmed Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title_short Mitochondrial-Endoplasmic Reticulum Communication-Mediated Oxidative Stress and Autophagy
title_sort mitochondrial-endoplasmic reticulum communication-mediated oxidative stress and autophagy
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9509228/
https://www.ncbi.nlm.nih.gov/pubmed/36164446
http://dx.doi.org/10.1155/2022/6459585
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