Endurance Exercise Ameliorates Aging-Related Bradyarrhythmia in Drosophila Resulting from miR-283 Knockdown in LN v s
Listed in
This article is not in any list yet, why not save it to one of your lists.Abstract
MicroRNAs (miRNAs) are crucial in regulating cardiac aging and related diseases, yet few functional miRNAs have been identified. Prior studies showed miR-216a upregulation in heart failure patients, but its impact on aging hearts is unknown. Our study revealed systemic miR-283 overexpression or knockdown caused age-related bradycardia, mimicking human bradyarrhythmia. Importantly, we found that knockdown of miR-283 in ventral-lateral neurons (LN v s), rather than in the heart, led to the occurrence of bradyarrhythmia, which was mainly caused by the upregulation of miR-283 expression in the whole brain and heart. The gene of clockwork orange ( cwo ) may mediate miR-283’s effect on heart rhythm. Additionally, to investigate the miRNA regulatory mechanism underlying exercise-induced delay in cardiac aging, we conducted a three-week endurance exercise program on miR-283 knockdown flies in LN v s. We found that exercise significantly downregulated the accumulation of miR-283 in the brain and myocardium caused by aging or miR-283 knockdown in LN v s, improved the structure of myocardial fibers, and effectively reduced bradyarrhythmia. Our findings provides a new perspective on distal neuromodulation and intervention in cardiac aging.
