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Mitochondria Dysfunction at the Heart of Viral Myocarditis : Mechanistic Insights and Therapeutic Implications Mohamud, Yasir; Li, Boaz; Bahreyni, Amirhossein; Luo, Honglin

Abstract

The myocardium/heart is the most mitochondria-rich tissue in the human body with mitochondria comprising approximately 30% of total cardiomyocyte volume. As the resident “powerhouse” of cells, mitochondria help to fuel the high energy demands of a continuously beating myocardium. It is no surprise that mitochondrial dysfunction underscores the pathogenesis of many cardiovascular ailments, including those of viral origin such as virus-induced myocarditis. Enteroviruses have been especially linked to injuries of the myocardium and its sequelae dilated cardiomyopathy for which no effective therapies currently exist. Intriguingly, recent mechanistic insights have demonstrated viral infections to directly damage mitochondria, impair the mitochondrial quality control processes of the cell, such as disrupting mitochondrial antiviral innate immune signaling, and promoting mitochondrial-dependent pathological inflammation of the infected myocardium. In this review, we briefly highlight recent insights on the virus-mitochondria crosstalk and discuss the therapeutic implications of targeting mitochondria to preserve heart function and ultimately combat viral myocarditis.

Item Metadata

Title
Mitochondria Dysfunction at the Heart of Viral Myocarditis : Mechanistic Insights and Therapeutic Implications
Creator
Mohamud, Yasir; Li, Boaz; Bahreyni, Amirhossein; Luo, Honglin
Contributor
Centre for Heart Lung Innovation; St. Paul's Hospital (Vancouver, B.C.)
Publisher
Multidisciplinary Digital Publishing Institute
Date Issued
2023-01-26
Description
The myocardium/heart is the most mitochondria-rich tissue in the human body with mitochondria comprising approximately 30% of total cardiomyocyte volume. As the resident “powerhouse” of cells, mitochondria help to fuel the high energy demands of a continuously beating myocardium. It is no surprise that mitochondrial dysfunction underscores the pathogenesis of many cardiovascular ailments, including those of viral origin such as virus-induced myocarditis. Enteroviruses have been especially linked to injuries of the myocardium and its sequelae dilated cardiomyopathy for which no effective therapies currently exist. Intriguingly, recent mechanistic insights have demonstrated viral infections to directly damage mitochondria, impair the mitochondrial quality control processes of the cell, such as disrupting mitochondrial antiviral innate immune signaling, and promoting mitochondrial-dependent pathological inflammation of the infected myocardium. In this review, we briefly highlight recent insights on the virus-mitochondria crosstalk and discuss the therapeutic implications of targeting mitochondria to preserve heart function and ultimately combat viral myocarditis.
Subject
apoptosis; autophagy; enterovirus; innate immune response; mitochondria; mitophagy; myocarditis
Genre
Article
Type
Text
Language
eng
Date Available
2025-06-23
Provider
Vancouver : University of British Columbia Library
Rights
CC BY 4.0
DOI
10.14288/1.0449169
URI
http://hdl.handle.net/2429/91404
Affiliation
Medicine, Faculty of; Pathology and Laboratory Medicine, Department of
Citation
Viruses 15 (2): 351 (2023)
Publisher DOI
10.3390/v15020351
Peer Review Status
Reviewed
Scholarly Level
Faculty; Researcher
Rights URI
https://creativecommons.org/licenses/by/4.0/
Aggregated Source Repository
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CC BY 4.0