Mitochondrial Mechanisms in Diabetic Cardiomyopathy.


Journal

Diabetes & metabolism journal
ISSN: 2233-6087
Titre abrégé: Diabetes Metab J
Pays: Korea (South)
ID NLM: 101556588

Informations de publication

Date de publication:
02 2020
Historique:
received: 15 10 2019
accepted: 20 12 2019
entrez: 26 2 2020
pubmed: 26 2 2020
medline: 16 6 2021
Statut: ppublish

Résumé

Mitochondrial medicine is increasingly discussed as a promising therapeutic approach, given that mitochondrial defects are thought to contribute to many prevalent diseases and their complications. In individuals with diabetes mellitus (DM), defects in mitochondrial structure and function occur in many organs throughout the body, contributing both to the pathogenesis of DM and complications of DM. Diabetic cardiomyopathy (DbCM) is increasingly recognized as an underlying cause of increased heart failure in DM, and several mitochondrial mechanisms have been proposed to contribute to the development of DbCM. Well established mechanisms include myocardial energy depletion due to impaired adenosine triphosphate (ATP) synthesis and mitochondrial uncoupling, and increased mitochondrial oxidative stress. A variety of upstream mechanisms of impaired ATP regeneration and increased mitochondrial reactive oxygen species have been proposed, and recent studies now also suggest alterations in mitochondrial dynamics and autophagy, impaired mitochondrial Ca²⁺ uptake, decreased cardiac adiponectin action, increased O-GlcNAcylation, and impaired activity of sirtuins to contribute to mitochondrial defects in DbCM, among others. In the current review, we present and discuss the evidence that underlies both established and recently proposed mechanisms that are thought to contribute to mitochondrial dysfunction in DbCM.

Identifiants

pubmed: 32097997
pii: 44.33
doi: 10.4093/dmj.2019.0185
pmc: PMC7043970
doi:

Substances chimiques

Reactive Oxygen Species 0
Sirtuins EC 3.5.1.-

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

33-53

Informations de copyright

Copyright © 2020 Korean Diabetes Association.

Déclaration de conflit d'intérêts

No potential conflict of interest relevant to this article was reported.

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Auteurs

Johannes Gollmer (J)

Division of Cardiology, Medical University of Graz, Graz, Austria.

Andreas Zirlik (A)

Division of Cardiology, Medical University of Graz, Graz, Austria.

Heiko Bugger (H)

Division of Cardiology, Medical University of Graz, Graz, Austria. heiko.bugger@medunigraz.at.

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