Identifying the potential therapeutic effects of miR‑6516 on muscle disuse atrophy

Abstract

Muscle atrophy is a debilitating condition with various causes; while aging is one of these causes, reduced engagement in routine muscle-strengthening activities also markedly contributes to muscle loss. Although extensive research has been conducted on microRNAs (miRNAs/miRs) and their associations with muscle atrophy, the roles played by miRNA precursors remain underexplored. The present study detected the upregulation of the miR-206 precursor in cell-free (cf)RNA from the plasma of patients at risk of sarcopenia, and in cfRNAs from the muscles of mice subjected to muscle atrophy. Additionally, a decline in the levels of the miR-6516 precursor was observed in mice with muscle atrophy. The administration of mimic-miR-6516 to mice immobilized due to injury inhibited muscle atrophy by targeting and inhibiting cyclin-dependent kinase inhibitor 1b (Cdkn1b). Based on these results, the miR-206 precursor appears to be a potential biomarker of muscle atrophy, whereas miR-6516 shows promise as a therapeutic target to alleviate muscle deterioration in patients with muscle disuse and atrophy.