Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus

There is increasing evidence that diabetic cardiomyopathy increases the risk of cardiac arrhythmia and sudden cardiac death. While the detailed mechanisms remain incompletely understood, the loss of mitochondrial function, which is often observed in the heart of patients with diabetes, has emerged a...

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Main Authors: Jiajia Song, Ruilin Yang, Jing Yang, Lufang Zhou
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-12-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fphys.2018.01670/full
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author Jiajia Song
Ruilin Yang
Ruilin Yang
Jing Yang
Lufang Zhou
author_facet Jiajia Song
Ruilin Yang
Ruilin Yang
Jing Yang
Lufang Zhou
author_sort Jiajia Song
collection DOAJ
description There is increasing evidence that diabetic cardiomyopathy increases the risk of cardiac arrhythmia and sudden cardiac death. While the detailed mechanisms remain incompletely understood, the loss of mitochondrial function, which is often observed in the heart of patients with diabetes, has emerged as a key contributor to the arrhythmogenic substrates. In this mini review, the pathophysiology of mitochondrial dysfunction in diabetes mellitus is explored in detail, followed by descriptions of several mechanisms potentially linking mitochondria to arrhythmogenesis in the context of diabetic cardiomyopathy.
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spelling doaj.art-532a929db23d440daea0d4caf18ba8dd2022-12-21T17:44:38ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2018-12-01910.3389/fphys.2018.01670420970Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes MellitusJiajia Song0Ruilin Yang1Ruilin Yang2Jing Yang3Lufang Zhou4Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesKey Laboratory of Mechanism Theory and Equipment Design of Ministry of Education, Tianjin University, Tianjin, ChinaDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesDivision of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL, United StatesThere is increasing evidence that diabetic cardiomyopathy increases the risk of cardiac arrhythmia and sudden cardiac death. While the detailed mechanisms remain incompletely understood, the loss of mitochondrial function, which is often observed in the heart of patients with diabetes, has emerged as a key contributor to the arrhythmogenic substrates. In this mini review, the pathophysiology of mitochondrial dysfunction in diabetes mellitus is explored in detail, followed by descriptions of several mechanisms potentially linking mitochondria to arrhythmogenesis in the context of diabetic cardiomyopathy.https://www.frontiersin.org/article/10.3389/fphys.2018.01670/fullmitochondrial dysfunctionarrhythmogenesisfibrosisredox signalingdiabetes
spellingShingle Jiajia Song
Ruilin Yang
Ruilin Yang
Jing Yang
Lufang Zhou
Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
Frontiers in Physiology
mitochondrial dysfunction
arrhythmogenesis
fibrosis
redox signaling
diabetes
title Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
title_full Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
title_fullStr Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
title_full_unstemmed Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
title_short Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus
title_sort mitochondrial dysfunction associated arrhythmogenic substrates in diabetes mellitus
topic mitochondrial dysfunction
arrhythmogenesis
fibrosis
redox signaling
diabetes
url https://www.frontiersin.org/article/10.3389/fphys.2018.01670/full
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AT ruilinyang mitochondrialdysfunctionassociatedarrhythmogenicsubstratesindiabetesmellitus
AT ruilinyang mitochondrialdysfunctionassociatedarrhythmogenicsubstratesindiabetesmellitus
AT jingyang mitochondrialdysfunctionassociatedarrhythmogenicsubstratesindiabetesmellitus
AT lufangzhou mitochondrialdysfunctionassociatedarrhythmogenicsubstratesindiabetesmellitus