Unloading/disuse induces skeletal muscle atrophy in bedridden patients and aged people, who cannot prevent it by means of exercise. Because interventions against known atrophy initiators, such as oxidative stress and neuronal NO synthase (nNOS) redistribution, are only partially effective, we investigated the involvement of melusin, a muscle‐specific integrin‐associated protein and a recognized regulator of protein kinases and mechanotransduction in cardiomyocytes.

中文翻译：

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melusin 的丢失是一种新的、神经元 NO 合酶/FoxO3 独立的主开关，它是卸载诱导的肌肉萎缩的主开关。

长期卧床不起的患者和老年人因负重/废用导致骨骼肌萎缩，无法通过运动来预防。因为对已知的萎缩起始因子的干预，如氧化应激和神经元 NO 合酶 (nNOS) 再分布，只是部分有效，我们研究了 melusin，一种肌肉特异性整合素相关蛋白和公认的蛋白激酶和机械转导调节剂的参与。心肌细胞。