Cellular and mitochondrial mechanisms of atrial fibrillation

2020 | journal article; overview. A publication with affiliation to the University of Göttingen.

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​Cellular and mitochondrial mechanisms of atrial fibrillation​
Mason, F. E. ; Pronto, J. R. D.; Alhussini, K.; Maack, C. & Voigt, N. ​ (2020) 
Basic Research in Cardiology115(6).​ DOI: https://doi.org/10.1007/s00395-020-00827-7 

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Authors
Mason, Fleur E. ; Pronto, Julius Ryan D.; Alhussini, Khaled; Maack, Christoph; Voigt, Niels 
Abstract
The molecular mechanisms underlying atrial fibrillation (AF), the most common form of arrhythmia, are poorly understood and therefore target-specific treatment options remain an unmet clinical need. Excitation–contraction coupling in cardiac myocytes requires high amounts of adenosine triphosphate (ATP), which is replenished by oxidative phosphorylation in mitochondria. Calcium (Ca2+) is a key regulator of mitochondrial function by stimulating the Krebs cycle, which produces nicotinamide adenine dinucleotide for ATP production at the electron transport chain and nicotinamide adenine dinucleotide phosphate for the elimination of reactive oxygen species (ROS). While it is now well established that mitochondrial dysfunction plays an important role in the pathophysiology of heart failure, this has been less investigated in atrial myocytes in AF. Considering the high prevalence of AF, investigating the role of mitochondria in this disease may guide the path towards new therapeutic targets. In this review, we discuss the importance of mitochondrial Ca2+ handling in regulating ATP production and mitochondrial ROS emission and how alterations, particularly in these aspects of mitochondrial activity, may play a role in AF. In addition to describing research advances, we highlight areas in which further studies are required to elucidate the role of mitochondria in AF.
Issue Date
2020
Journal
Basic Research in Cardiology 
Project
EXC 2067: Multiscale Bioimaging 
SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz 
SFB 1002 | A13: Bedeutung einer gestörten zytosolischen Calciumpufferung bei der atrialen Arrhythmogenese bei Patienten mit Herzinsuffizienz (HF) 
Working Group
RG Voigt (Molecular Pharmacology) 
ISSN
0300-8428
eISSN
1435-1803
Language
English
Sponsor
Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659
Else Kröner-Fresenius-Stiftung http://dx.doi.org/10.13039/501100003042
Deutsches Zentrum für Herz-Kreislaufforschung http://dx.doi.org/10.13039/100010447
Bundesministerium für Bildung und Forschung http://dx.doi.org/10.13039/501100002347
Georg-August-Universität Göttingen (1018)

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