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Cellular and mitochondrial mechanisms of atrial fibrillation

Fleur E Mason1,2, Julius Ryan D Pronto1,2, Khaled Alhussini3

  • 1Institute of Pharmacology and Toxicology, University Medical Center Göttingen, Georg-August University Göttingen, Robert-Koch-Straße 40, 37075, Göttingen, Germany.

Basic Research in Cardiology
|December 1, 2020
PubMed

Insights

Mitochondrial dysfunction, specifically in calcium handling, may contribute to atrial fibrillation (AF). Understanding these mechanisms could lead to new treatments for this common heart arrhythmia.

Area of Science:

  • Cardiology
  • Mitochondrial Biology
  • Electrophysiology

Background:

  • Atrial fibrillation (AF) is a prevalent arrhythmia with poorly understood molecular mechanisms, limiting targeted therapies.
  • Mitochondria are crucial for cardiac myocyte energy production (ATP) via oxidative phosphorylation.
  • Mitochondrial calcium (Ca2+) regulates ATP synthesis and reactive oxygen species (ROS) elimination, but its role in AF is under-investigated.

Purpose of the Study:

  • To review the role of mitochondrial calcium handling in ATP production and ROS emission in atrial myocytes.
  • To explore how alterations in mitochondrial function may contribute to the pathophysiology of atrial fibrillation.
  • To identify knowledge gaps and guide future research on mitochondria in AF.

Main Methods:

  • Literature review focusing on mitochondrial Ca2+ handling, ATP production, and ROS in the context of AF.
  • Analysis of existing research on mitochondrial dysfunction in heart failure and its potential relevance to AF.
  • Synthesis of current understanding and identification of areas requiring further investigation.

Main Results:

  • Mitochondrial Ca2+ is a key regulator of energy metabolism and oxidative stress within cardiac cells.
  • Dysfunctional mitochondrial Ca2+ handling is implicated in cellular processes relevant to AF pathophysiology.
  • Altered ATP production and ROS emission by mitochondria are potential contributors to AF.

Conclusions:

  • Mitochondrial Ca2+ dysregulation is a plausible mechanism contributing to atrial fibrillation.
  • Further research into mitochondrial function in atrial myocytes is essential for developing novel AF therapies.
  • Targeting mitochondrial pathways represents a promising avenue for future AF treatment strategies.
Keywords:
Atrial cardiomyopathyAtrial fibrillationCalciumElectrophysiologyMitochondriaOxidative stress

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