IMR Press / FBL / Volume 22 / Issue 7 / DOI: 10.2741/4541

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Review

Mitochondrial DNA, mitochondrial dysfunction, and cardiac manifestations

Show Less
1 Department of Integrated Biomedical Science, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea
2 National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University, Busan 47392, Korea
3 Department of Physiology and Pathophysiology, Tianjin Medical University, Tainjin 300070, P.R. China

Academic Editor: Myung-Shik Lee

Front. Biosci. (Landmark Ed) 2017, 22(7), 1177–1194; https://doi.org/10.2741/4541
Published: 1 March 2017
(This article belongs to the Special Issue Mitochondrial dysfunction in chronic disease)
Abstract

Mitochondria, are the powerhouses of cells, have their own DNA (mtDNA), regulate the transport of metabolites and ions, and impact cell physiology, survival, and death. Mitochondrial dysfunction, including impaired oxidative phosphorylation, preferentially affects heart function due to an imbalance of energy supply and demand. Recently, mitochondrial mutations and associated mitochondrial dysfunction were suggested as a causal factor of cardiac manifestations. Oxidative stress largely influences mtDNA stability due to oxidative modifications of mtDNA. Furthermore, the continuous replicative state of mtDNA and presence of minimal nucleoid structure render mitochondria vulnerable to oxidative damage and subsequent mutations, which impair mitochondrial functions. However, the occurrence of mtDNA heteroplasmy in the same mitochondrion or cell and presence of nuclear DNA-encoded mtDNA repair systems raise questions regarding whether oxidative stress–mediated mtDNA mutations are the major driving force in accumulation of mtDNA mutations. Here, we address the possible causes of mitochondrial DNA mutations and their involvement in cardiac manifestations. Current strategies for treatment related to mitochondrial mutations and/or dysfunction in cardiac manifestations are briefly discussed.

Keywords
Cardiac Manifestations
Mitochondria
Mutation
Maintenance
Mitochondrial DNA
Review
Share
Back to top