The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes
Mitochondrial dysfunction is known to be associated with a wide range of human pathologies, such as cancer, metabolic, and cardiovascular diseases. One of the possible ways of mitochondrial involvement in the cellular damage is excessive production of reactive oxygen and nitrogen species (ROS and RN...
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doaj-e356fce9c9ad46e4ae4781af480f69572021-05-07T08:48:55ZengFrontiers Media S.A.Frontiers in Molecular Biosciences2296-889X2021-05-01810.3389/fmolb.2021.671908671908The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and DiabetesOlga A. Zhunina0Nikita G. Yabbarov1Andrey V. Grechko2Antonina V. Starodubova3Ekaterina Ivanova4Nikita G. Nikiforov5Nikita G. Nikiforov6Nikita G. Nikiforov7Alexander N. Orekhov8Alexander N. Orekhov9Chemical Biology Department, Russian Research Center for Molecular Diagnostics and Therapy, Moscow, RussiaChemical Biology Department, Russian Research Center for Molecular Diagnostics and Therapy, Moscow, RussiaFederal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, Moscow, RussiaFederal Research Centre for Nutrition, Biotechnology and Food Safety, Moscow, RussiaDepartment of Basic Research, Skolkovo Innovative Center, Institute for Atherosclerosis Research, Moscow, RussiaNational Medical Research Center of Cardiology, Institute of Experimental Cardiology, Moscow, RussiaInstitute of Gene Biology, Moscow, RussiaLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, Moscow, RussiaLaboratory of Cellular and Molecular Pathology of Cardiovascular System, Institute of Human Morphology, Moscow, RussiaLaboratory of Angiopathology, Institute of General Pathology and Pathophysiology, Moscow, RussiaMitochondrial dysfunction is known to be associated with a wide range of human pathologies, such as cancer, metabolic, and cardiovascular diseases. One of the possible ways of mitochondrial involvement in the cellular damage is excessive production of reactive oxygen and nitrogen species (ROS and RNS) that cannot be effectively neutralized by existing antioxidant systems. In mitochondria, ROS and RNS can contribute to protein and mitochondrial DNA (mtDNA) damage causing failure of enzymatic chains and mutations that can impair mitochondrial function. These processes further lead to abnormal cell signaling, premature cell senescence, initiation of inflammation, and apoptosis. Recent studies have identified numerous mtDNA mutations associated with different human pathologies. Some of them result in imbalanced oxidative phosphorylation, while others affect mitochondrial protein synthesis. In this review, we discuss the role of mtDNA mutations in cancer, diabetes, cardiovascular diseases, and atherosclerosis. We provide a list of currently described mtDNA mutations associated with each pathology and discuss the possible future perspective of the research.https://www.frontiersin.org/articles/10.3389/fmolb.2021.671908/fullatherosclerosiscancerdiabetesDNA damagemitochondriareactive oxygen species |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Olga A. Zhunina Nikita G. Yabbarov Andrey V. Grechko Antonina V. Starodubova Ekaterina Ivanova Nikita G. Nikiforov Nikita G. Nikiforov Nikita G. Nikiforov Alexander N. Orekhov Alexander N. Orekhov |
spellingShingle |
Olga A. Zhunina Nikita G. Yabbarov Andrey V. Grechko Antonina V. Starodubova Ekaterina Ivanova Nikita G. Nikiforov Nikita G. Nikiforov Nikita G. Nikiforov Alexander N. Orekhov Alexander N. Orekhov The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes Frontiers in Molecular Biosciences atherosclerosis cancer diabetes DNA damage mitochondria reactive oxygen species |
author_facet |
Olga A. Zhunina Nikita G. Yabbarov Andrey V. Grechko Antonina V. Starodubova Ekaterina Ivanova Nikita G. Nikiforov Nikita G. Nikiforov Nikita G. Nikiforov Alexander N. Orekhov Alexander N. Orekhov |
author_sort |
Olga A. Zhunina |
title |
The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes |
title_short |
The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes |
title_full |
The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes |
title_fullStr |
The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes |
title_full_unstemmed |
The Role of Mitochondrial Dysfunction in Vascular Disease, Tumorigenesis, and Diabetes |
title_sort |
role of mitochondrial dysfunction in vascular disease, tumorigenesis, and diabetes |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Molecular Biosciences |
issn |
2296-889X |
publishDate |
2021-05-01 |
description |
Mitochondrial dysfunction is known to be associated with a wide range of human pathologies, such as cancer, metabolic, and cardiovascular diseases. One of the possible ways of mitochondrial involvement in the cellular damage is excessive production of reactive oxygen and nitrogen species (ROS and RNS) that cannot be effectively neutralized by existing antioxidant systems. In mitochondria, ROS and RNS can contribute to protein and mitochondrial DNA (mtDNA) damage causing failure of enzymatic chains and mutations that can impair mitochondrial function. These processes further lead to abnormal cell signaling, premature cell senescence, initiation of inflammation, and apoptosis. Recent studies have identified numerous mtDNA mutations associated with different human pathologies. Some of them result in imbalanced oxidative phosphorylation, while others affect mitochondrial protein synthesis. In this review, we discuss the role of mtDNA mutations in cancer, diabetes, cardiovascular diseases, and atherosclerosis. We provide a list of currently described mtDNA mutations associated with each pathology and discuss the possible future perspective of the research. |
topic |
atherosclerosis cancer diabetes DNA damage mitochondria reactive oxygen species |
url |
https://www.frontiersin.org/articles/10.3389/fmolb.2021.671908/full |
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