Abstract
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.
Highlights
These findings indicate that Atrial fibrillation (AF) drives the release of mitochondrial DNA from the cardiomyocytes into the circulation, thereby representing a potential biomarker for the stage of AF and predict recurrence after AF treatment
As current treatments are not directed at the underlying pathophysiological processes driving AF, research is increasingly focused on the dissection of the molecular mechanisms
Mitochondrial dysfunction has been recently identified as a contributing factor in the electropathology of AF
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Several therapeutic approaches have been developed, including pharmacotherapy [9] As these treatments are directed at electrical changes and not the underlying structural disruption, they are only moderately effective to attenuate AF [5]. The by-product of mitochondrial bioenergetic activity is the generation of reactive oxygen species (ROS) [15] These toxic and damaging by-products are neutralized or scavenged by antioxidants. DNA damage are increased in patients with AF [20] This contributes to the impairment of the bioenergetic function of mitochondria and the onset and progression of AF [21,22]. We elaborate on key mitochondrial modulators as a potential biomarker in clinical AF
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
