The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery

Atrial fibrillation (AF) is the most prevalent and progressive cardiac arrhythmia worldwide and is associated with serious complications such as heart failure and ischemic stroke. Current treatment modalities attenuate AF symptoms and are only moderately effective in halting the arrhythmia. Therefor...

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Main Authors: Lisa Pool, Leonoor F. J. M. Wijdeveld, Natasja M. S. de Groot, Bianca J. J. M. Brundel
Format: Article
Language:English
Published: MDPI AG 2021-08-01
Series:International Journal of Molecular Sciences
Subjects:
Online Access:https://www.mdpi.com/1422-0067/22/16/8463
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author Lisa Pool
Leonoor F. J. M. Wijdeveld
Natasja M. S. de Groot
Bianca J. J. M. Brundel
author_facet Lisa Pool
Leonoor F. J. M. Wijdeveld
Natasja M. S. de Groot
Bianca J. J. M. Brundel
author_sort Lisa Pool
collection DOAJ
description Atrial fibrillation (AF) is the most prevalent and progressive cardiac arrhythmia worldwide and is associated with serious complications such as heart failure and ischemic stroke. Current treatment modalities attenuate AF symptoms and are only moderately effective in halting the arrhythmia. Therefore, there is an urgent need to dissect molecular mechanisms that drive AF. As AF is characterized by a rapid atrial activation rate, which requires a high energy metabolism, a role of mitochondrial dysfunction in AF pathophysiology is plausible. It is well known that mitochondria play a central role in cardiomyocyte function, as they produce energy to support the mechanical and electrical function of the heart. Details on the molecular mechanisms underlying mitochondrial dysfunction are increasingly being uncovered as a contributing factor in the loss of cardiomyocyte function and AF. Considering the high prevalence of AF, investigating the role of mitochondrial impairment in AF may guide the path towards new therapeutic and diagnostic targets. In this review, the latest evidence on the role of mitochondria dysfunction in AF is presented. We highlight the key modulators of mitochondrial dysfunction that drive AF and discuss whether they represent potential targets for therapeutic interventions and diagnostics in clinical AF.
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spelling doaj.art-06d9169de9864094a85d581a8783c54b2023-11-22T07:55:27ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672021-08-012216846310.3390/ijms22168463The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker DiscoveryLisa Pool0Leonoor F. J. M. Wijdeveld1Natasja M. S. de Groot2Bianca J. J. M. Brundel3Department of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The NetherlandsDepartment of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The NetherlandsErasmus Medical Center, Department of Cardiology, 3015 GD Rotterdam, The NetherlandsDepartment of Physiology, Amsterdam Cardiovascular Sciences, Amsterdam UMC, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The NetherlandsAtrial fibrillation (AF) is the most prevalent and progressive cardiac arrhythmia worldwide and is associated with serious complications such as heart failure and ischemic stroke. Current treatment modalities attenuate AF symptoms and are only moderately effective in halting the arrhythmia. Therefore, there is an urgent need to dissect molecular mechanisms that drive AF. As AF is characterized by a rapid atrial activation rate, which requires a high energy metabolism, a role of mitochondrial dysfunction in AF pathophysiology is plausible. It is well known that mitochondria play a central role in cardiomyocyte function, as they produce energy to support the mechanical and electrical function of the heart. Details on the molecular mechanisms underlying mitochondrial dysfunction are increasingly being uncovered as a contributing factor in the loss of cardiomyocyte function and AF. Considering the high prevalence of AF, investigating the role of mitochondrial impairment in AF may guide the path towards new therapeutic and diagnostic targets. In this review, the latest evidence on the role of mitochondria dysfunction in AF is presented. We highlight the key modulators of mitochondrial dysfunction that drive AF and discuss whether they represent potential targets for therapeutic interventions and diagnostics in clinical AF.https://www.mdpi.com/1422-0067/22/16/8463atrial fibrillationmitochondriaelectrophysiologyatrial cardiomyopathydiagnosticsbiomarker
spellingShingle Lisa Pool
Leonoor F. J. M. Wijdeveld
Natasja M. S. de Groot
Bianca J. J. M. Brundel
The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
International Journal of Molecular Sciences
atrial fibrillation
mitochondria
electrophysiology
atrial cardiomyopathy
diagnostics
biomarker
title The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
title_full The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
title_fullStr The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
title_full_unstemmed The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
title_short The Role of Mitochondrial Dysfunction in Atrial Fibrillation: Translation to Druggable Target and Biomarker Discovery
title_sort role of mitochondrial dysfunction in atrial fibrillation translation to druggable target and biomarker discovery
topic atrial fibrillation
mitochondria
electrophysiology
atrial cardiomyopathy
diagnostics
biomarker
url https://www.mdpi.com/1422-0067/22/16/8463
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