Key result
Aerobic exercise training appears to modulate miRNA-16-5p and miRNA-26a-5p expression, activating Akt/mTOR pathways to produce physiological left ventricular hypertrophy.
Why the study?
New insight into mTOR signaling-related microRNA mechanisms in exercise training can aid understanding of physiological LVH and potential therapeutic applications.
Understanding the miRNA-mediated molecular basis of physiological cardiac hypertrophy could provide insights for future therapeutic applications.
Physiological hypertrophic growth of the heart as a compensatory response to exercise training (ET) is coupled with recent progress in dissecting the microRNA (miRNA)-mediated molecular basis of hypertrophy. Aerobic ET seems to reduce miRNA-16-5p and increase miRNA-26a-5p expression in a volume-dependent mode, activating protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathways, and likely produces an enhanced left ventricular hypertrophy (LVH) in high-volume endurance training. New insight into these mechanisms can be useful in understanding physiological LVH and how it might be harnessed as a therapeutic application.
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Pelozin et al. (2021) conducted a review in Physiological left ventricular hypertrophy. Aerobic exercise training (high-volume endurance training) was evaluated. Aerobic exercise training appears to modulate miRNA-16-5p and miRNA-26a-5p expression, activating Akt/mTOR pathways to produce physiological left ventricular hypertrophy.
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