Back

Endurance Exercise Ameliorates Aging-Related Bradyarrhythmia in Drosophila Resulting from miR-283 Knockdown in LNvs

Li, Q.; Ping, X.; Yu, Z.; Yi, Q.; Tang, C.; Wang, X.; Zheng, L.

2025-03-01 physiology
10.1101/2025.02.25.640161 bioRxiv
Show 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 (LNvs), 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-283s 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 LNvs. We found that exercise significantly downregulated the accumulation of miR-283 in the brain and myocardium caused by aging or miR-283 knockdown in LNvs, improved the structure of myocardial fibers, and effectively reduced bradyarrhythmia. Our findings provides a new perspective on distal neuromodulation and intervention in cardiac aging.

Matching journals

The top 4 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.