Mitochondrial dysfunction in cardiovascular disease: Current status of translational research/clinical and therapeutic implications

Journal article


Manolis, A., Manolis, Antonis A., Manolis, Theodora A., Apostolaki, Naomi E., Apostolopoulos, Evdoxia J., Melita, Helen and Katsiki, Niki 2020. Mitochondrial dysfunction in cardiovascular disease: Current status of translational research/clinical and therapeutic implications. Medicinal Research Reviews. 41 (1), pp. 275-313. https://doi.org/10.1002/med.21732
AuthorsManolis, A., Manolis, Antonis A., Manolis, Theodora A., Apostolaki, Naomi E., Apostolopoulos, Evdoxia J., Melita, Helen and Katsiki, Niki
Abstract

Mitochondria provide energy to the cell during aerobic respiration by supplying ~95% of the adenosine triphosphate (ATP) molecules via oxidative phosphorylation. These organelles have various other functions, all carried out by numerous proteins, with the majority of them being encoded by nuclear DNA (nDNA). Mitochondria occupy ~1/3 of the volume of myocardial cells in adults, and function at levels of high-efficiency to promptly meet the energy requirements of the myocardial contractile units. Mitochondria have their own DNA (mtDNA), which contains 37 genes and is maternally inherited. Over the last several years, a variety of functions of these organelles have been discovered and this has led to a growing interest in their involvement in various diseases, including cardiovascular (CV) diseases. Mitochondrial dysfunction relates to the status where mitochondria cannot meet the demands of a cell for ATP and there is an enhanced formation of reactive-oxygen species. This dysfunction may occur as a result of mtDNA and/or nDNA mutations, but also as a response to aging and various disease and environmental stresses, leading to the development of cardiomyopathies and other CV diseases. Designing mitochondria-targeted therapeutic strategies aiming to maintain or restore mitochondrial function has been a great challenge as a result of variable responses according to the etiology of the disorder. There have been several preclinical data on such therapies, but clinical studies are scarce. A major challenge relates to the techniques needed to eclectically deliver the therapeutic agents to cardiac tissues and to damaged mitochondria for successful clinical outcomes. All these issues and progress made over the last several years are herein reviewed.

KeywordsMolecular medicine; Pharmacology; Drug discovery
Year2020
JournalMedicinal Research Reviews
Journal citation41 (1), pp. 275-313
PublisherWiley
ISSN0198-6325
1098-1128
Digital Object Identifier (DOI)https://doi.org/10.1002/med.21732
Official URLhttps://onlinelibrary.wiley.com/doi/epdf/10.1002/med.21732
Publication dates
Online21 Sep 2020
Publication process dates
Deposited15 Jul 2021
Output statusPublished
Licensehttp://onlinelibrary.wiley.com/termsAndConditions#vor
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