Skeletal muscle has great plasticity. An increase in protein degradation can cause muscle atrophy. Atrogin-1 and muscle ring finger-1 (MuRF1) are dramatically upregulated in various muscle atrophy. Inhibition of Atrogin-1 and MuRF1 protects against muscle atrophy. MiR-29 plays an important regulatory role in skeletal muscle development. However, the function of miR-29 in skeletal muscle protein metabolism is not clear. To investigate the function of miR-29, we generated miR-29 knockout mice and the miR-29ab1 cluster overexpression mice. The disruption of miR-29 led to severe atrophy of skeletal muscle during puberty, and the muscle-specific overexpression of the miR-29ab1 cluster protected against denervation-induced and fasting-induced muscle atrophy. Furthermore, the overexpression of miR-29a, b mimics in myotubes resisted the muscle atrophy. MuRF1 was the direct target gene of miR-29a, b. These results demonstrate that miR-29ab1 cluster plays a critical role in the maintenance of skeletal muscle. MiR-29ab1 cluster is the excellent inhibitor of MuRF1, ultimately indicating that miR-29ab1 cluster is good therapeutic molecule candidate for adulthood.

中文翻译：

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MiR-29ab1 簇通过抑制 MuRF1 来抵抗肌肉萎缩

骨骼肌具有很大的可塑性。蛋白质降解的增加会导致肌肉萎缩。Atrogin-1 和无名指肌肉 1 (MuRF1) 在各种肌肉萎缩中显着上调。抑制 Atrogin-1 和 MuRF1 可防止肌肉萎缩。MiR-29 在骨骼肌发育中起着重要的调节作用。然而，miR-29在骨骼肌蛋白代谢中的功能尚不清楚。为了研究 miR-29 的功能，我们生成了 miR-29 敲除小鼠和 miR-29ab1 簇过表达小鼠。miR-29 的破坏导致青春期骨骼肌严重萎缩，而 miR-29ab1 簇的肌肉特异性过表达可防止去神经支配和禁食诱导的肌肉萎缩。此外，miR-29a、b 模拟物在肌管中的过表达抵抗了肌肉萎缩。MuRF1 是 miR-29a、b 的直接靶基因。这些结果表明 miR-29ab1 簇在骨骼肌的维持中起着关键作用。MiR-29ab1 簇是 MuRF1 的优秀抑制剂，最终表明 miR-29ab1 簇是成年期良好的治疗分子候选者。