Sarcoplasmic reticulum-mitochondria communication; implications for cardiac arrhythmia
Shanna Hamilton1, Radmila Terentyeva1, Richard T Clements2
1Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, Wexner Medical Center, The Ohio State University, Columbus, OH, United States of America.
Journal of Molecular and Cellular Cardiology
|April 15, 2021
Summary
Sudden cardiac death from ventricular arrhythmias is a global concern. This review explores how impaired communication between mitochondria and calcium release channels increases heart disease risk.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Sudden cardiac death (SCD) due to ventricular tachyarrhythmias is a leading global cause of mortality.
- Conditions like heart failure, diabetic cardiomyopathy, aging, and inherited disorders elevate the risk of malignant cardiac arrhythmias.
- Defective mitochondrial function and disrupted intracellular calcium (Ca2+) handling are key contributors to cardiac pathophysiology and arrhythmogenesis.
Purpose of the Study:
- To review current understanding of the bidirectional control between ryanodine receptor-mediated sarcoplasmic reticulum Ca2+ release and mitochondrial function.
- To elucidate how impaired crosstalk between these organelles contributes to increased arrhythmic risk in cardiac disease.
Main Methods:
- Literature review of current scientific advances.
- Analysis of the interplay between mitochondrial function and calcium homeostasis in the heart.
- Examination of the role of sarcoplasmic reticulum Ca2+ release in arrhythmogenesis.
Main Results:
- The article details the intricate bidirectional control mechanisms linking mitochondrial function and ryanodine receptor activity.
- Evidence highlights that defects in the crosstalk between mitochondria and the sarcoplasmic reticulum's Ca2+ release channels are critical in promoting cardiac arrhythmias.
- Dysregulation of Ca2+ handling and mitochondrial energetics significantly impacts cardiac electrical stability.
Conclusions:
- Impaired communication between mitochondria and sarcoplasmic reticulum Ca2+ release channels is a significant factor in the development of life-threatening cardiac arrhythmias.
- Targeting the crosstalk between these organelles may offer novel therapeutic strategies for preventing sudden cardiac death in patients with heart disease.
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