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Mitochondrial DNA abnormalities and metabolic syndrome

Metabolic syndrome (MetS) is a complex pathological condition that involves disrupted carbohydrate, protein, and fat metabolism in the human body, and is a major risk factor for several chronic diseases, including diabetes, cardiovascular disease, and cerebrovascular disease. While the exact pathoge...

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Autores principales: Ding, Xudong, Fang, Tingting, Pang, Xiaoqi, Pan, Xueru, Tong, Aiying, Lin, Ziyi, Zheng, Shikuan, Zheng, Ningning
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10036395/
https://www.ncbi.nlm.nih.gov/pubmed/36968196
http://dx.doi.org/10.3389/fcell.2023.1153174
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author Ding, Xudong
Fang, Tingting
Pang, Xiaoqi
Pan, Xueru
Tong, Aiying
Lin, Ziyi
Zheng, Shikuan
Zheng, Ningning
author_facet Ding, Xudong
Fang, Tingting
Pang, Xiaoqi
Pan, Xueru
Tong, Aiying
Lin, Ziyi
Zheng, Shikuan
Zheng, Ningning
author_sort Ding, Xudong
collection PubMed
description Metabolic syndrome (MetS) is a complex pathological condition that involves disrupted carbohydrate, protein, and fat metabolism in the human body, and is a major risk factor for several chronic diseases, including diabetes, cardiovascular disease, and cerebrovascular disease. While the exact pathogenesis of metabolic syndrome is not yet fully understood, there is increasing evidence linking mitochondrial dysfunction, which is closely related to the mitochondrial genome and mitochondrial dynamics, to the development of this condition. Recent advancements in genetic sequencing technologies have allowed for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with metabolic syndrome. Additionally, the identification of specific mechanisms by which reduced mtDNA copy number and gene mutations, as well as abnormalities in mtDNA-encoded proteins and mitochondrial dynamics, contribute to metabolic syndrome may promote the development of novel therapeutic targets and interventions, such as the restoration of mitochondrial function through the targeting of specific mitochondrial defects. Additionally, advancements in genetic sequencing technologies may allow for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with MetS. Therefore, strategies to promote the restoration of mitochondrial function by addressing these defects may offer new options for treating MetS. This review provides an overview of the research progress and significance of mitochondrial genome and mitochondrial dynamics in MetS.
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spelling pubmed-100363952023-03-25 Mitochondrial DNA abnormalities and metabolic syndrome Ding, Xudong Fang, Tingting Pang, Xiaoqi Pan, Xueru Tong, Aiying Lin, Ziyi Zheng, Shikuan Zheng, Ningning Front Cell Dev Biol Cell and Developmental Biology Metabolic syndrome (MetS) is a complex pathological condition that involves disrupted carbohydrate, protein, and fat metabolism in the human body, and is a major risk factor for several chronic diseases, including diabetes, cardiovascular disease, and cerebrovascular disease. While the exact pathogenesis of metabolic syndrome is not yet fully understood, there is increasing evidence linking mitochondrial dysfunction, which is closely related to the mitochondrial genome and mitochondrial dynamics, to the development of this condition. Recent advancements in genetic sequencing technologies have allowed for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with metabolic syndrome. Additionally, the identification of specific mechanisms by which reduced mtDNA copy number and gene mutations, as well as abnormalities in mtDNA-encoded proteins and mitochondrial dynamics, contribute to metabolic syndrome may promote the development of novel therapeutic targets and interventions, such as the restoration of mitochondrial function through the targeting of specific mitochondrial defects. Additionally, advancements in genetic sequencing technologies may allow for more accurate detection of mtDNA mutations and other mitochondrial abnormalities, leading to earlier diagnosis and intervention in patients with MetS. Therefore, strategies to promote the restoration of mitochondrial function by addressing these defects may offer new options for treating MetS. This review provides an overview of the research progress and significance of mitochondrial genome and mitochondrial dynamics in MetS. Frontiers Media S.A. 2023-03-10 /pmc/articles/PMC10036395/ /pubmed/36968196 http://dx.doi.org/10.3389/fcell.2023.1153174 Text en Copyright © 2023 Ding, Fang, Pang, Pan, Tong, Lin, Zheng and Zheng. 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 Cell and Developmental Biology
Ding, Xudong
Fang, Tingting
Pang, Xiaoqi
Pan, Xueru
Tong, Aiying
Lin, Ziyi
Zheng, Shikuan
Zheng, Ningning
Mitochondrial DNA abnormalities and metabolic syndrome
title Mitochondrial DNA abnormalities and metabolic syndrome
title_full Mitochondrial DNA abnormalities and metabolic syndrome
title_fullStr Mitochondrial DNA abnormalities and metabolic syndrome
title_full_unstemmed Mitochondrial DNA abnormalities and metabolic syndrome
title_short Mitochondrial DNA abnormalities and metabolic syndrome
title_sort mitochondrial dna abnormalities and metabolic syndrome
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10036395/
https://www.ncbi.nlm.nih.gov/pubmed/36968196
http://dx.doi.org/10.3389/fcell.2023.1153174
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