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The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications

Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycaemia, with absolute insulin deficiency or insulin resistance as the main cause, and causes damage to various target organs including the heart, kidney and neurovascular. In terms of the pathological and physiological me...

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Autores principales: Zhang, Ziwei, Huang, Qingxia, Zhao, Daqing, Lian, Fengmei, Li, Xiangyan, Qi, Wenxiu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9941188/
https://www.ncbi.nlm.nih.gov/pubmed/36824356
http://dx.doi.org/10.3389/fendo.2023.1112363
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author Zhang, Ziwei
Huang, Qingxia
Zhao, Daqing
Lian, Fengmei
Li, Xiangyan
Qi, Wenxiu
author_facet Zhang, Ziwei
Huang, Qingxia
Zhao, Daqing
Lian, Fengmei
Li, Xiangyan
Qi, Wenxiu
author_sort Zhang, Ziwei
collection PubMed
description Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycaemia, with absolute insulin deficiency or insulin resistance as the main cause, and causes damage to various target organs including the heart, kidney and neurovascular. In terms of the pathological and physiological mechanisms of DM, oxidative stress is one of the main mechanisms leading to DM and is an important link between DM and its complications. Oxidative stress is a pathological phenomenon resulting from an imbalance between the production of free radicals and the scavenging of antioxidant systems. The main site of reactive oxygen species (ROS) production is the mitochondria, which are also the main organelles damaged. In a chronic high glucose environment, impaired electron transport chain within the mitochondria leads to the production of ROS, prompts increased proton leakage and altered mitochondrial membrane potential (MMP), which in turn releases cytochrome c (cyt-c), leading to apoptosis. This subsequently leads to a vicious cycle of impaired clearance by the body’s antioxidant system, impaired transcription and protein synthesis of mitochondrial DNA (mtDNA), which is responsible for encoding mitochondrial proteins, and impaired DNA repair systems, contributing to mitochondrial dysfunction. This paper reviews the dysfunction of mitochondria in the environment of high glucose induced oxidative stress in the DM model, and looks forward to providing a new treatment plan for oxidative stress based on mitochondrial dysfunction.
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spelling pubmed-99411882023-02-22 The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications Zhang, Ziwei Huang, Qingxia Zhao, Daqing Lian, Fengmei Li, Xiangyan Qi, Wenxiu Front Endocrinol (Lausanne) Endocrinology Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycaemia, with absolute insulin deficiency or insulin resistance as the main cause, and causes damage to various target organs including the heart, kidney and neurovascular. In terms of the pathological and physiological mechanisms of DM, oxidative stress is one of the main mechanisms leading to DM and is an important link between DM and its complications. Oxidative stress is a pathological phenomenon resulting from an imbalance between the production of free radicals and the scavenging of antioxidant systems. The main site of reactive oxygen species (ROS) production is the mitochondria, which are also the main organelles damaged. In a chronic high glucose environment, impaired electron transport chain within the mitochondria leads to the production of ROS, prompts increased proton leakage and altered mitochondrial membrane potential (MMP), which in turn releases cytochrome c (cyt-c), leading to apoptosis. This subsequently leads to a vicious cycle of impaired clearance by the body’s antioxidant system, impaired transcription and protein synthesis of mitochondrial DNA (mtDNA), which is responsible for encoding mitochondrial proteins, and impaired DNA repair systems, contributing to mitochondrial dysfunction. This paper reviews the dysfunction of mitochondria in the environment of high glucose induced oxidative stress in the DM model, and looks forward to providing a new treatment plan for oxidative stress based on mitochondrial dysfunction. Frontiers Media S.A. 2023-02-07 /pmc/articles/PMC9941188/ /pubmed/36824356 http://dx.doi.org/10.3389/fendo.2023.1112363 Text en Copyright © 2023 Zhang, Huang, Zhao, Lian, Li and Qi https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Endocrinology
Zhang, Ziwei
Huang, Qingxia
Zhao, Daqing
Lian, Fengmei
Li, Xiangyan
Qi, Wenxiu
The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title_full The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title_fullStr The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title_full_unstemmed The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title_short The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
title_sort impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications
topic Endocrinology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9941188/
https://www.ncbi.nlm.nih.gov/pubmed/36824356
http://dx.doi.org/10.3389/fendo.2023.1112363
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