Department of Pharmacology, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Department of Neurosurgery, Institute for Cancer Research, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.
Mol Med Rep. 2024 Jul;30(1). doi: 10.3892/mmr.2024.13243. Epub 2024 May 17.
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.
肌肉萎缩是一种具有多种病因的衰弱性疾病；虽然衰老就是其中的一个病因，但日常肌肉强化活动的减少也会显著导致肌肉丧失。尽管已经对 microRNAs（miRNAs/miRs）及其与肌肉萎缩的关联进行了广泛的研究，但 miRNA 前体的作用仍未得到充分探索。本研究在易发生肌肉减少症的患者的血浆无细胞（cf）RNA 以及肌肉萎缩小鼠的 cfRNAs 中检测到 miR-206 前体的上调。此外，在肌肉萎缩的小鼠中观察到 miR-6516 前体的水平下降。用模拟 miR-6516 处理因受伤而固定不动的小鼠，通过靶向和抑制细胞周期蛋白依赖性激酶抑制剂 1b () 来抑制肌肉萎缩。基于这些结果，miR-206 前体似乎是肌肉萎缩的潜在生物标志物，而 miR-6516 有望成为治疗靶点，以缓解肌肉失用和萎缩患者的肌肉恶化。
