Identifying the Potential Therapeutic Effects of MiR‑6516 on Muscle Disuse Atrophy

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 (). 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.