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Skeletal Muscle Pathophysiology: The Emerging Role of Spermine Oxidase and Spermidine

机译：骨骼肌病理生理学：精胺氧化酶和亚精胺的新兴作用

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Skeletal muscle comprises approximately 40% of the total body mass. Preserving muscle health and function is essential for the entire body in order to counteract chronic diseases such as type II diabetes, cardiovascular diseases, and cancer. Prolonged physical inactivity, particularly among the elderly, causes muscle atrophy, a pathological state with adverse outcomes such as poor quality of life, physical disability, and high mortality. In murine skeletal muscle C2C12 cells, increased expression of the spermine oxidase (SMOX) enzyme has been found during cell differentiation. Notably, SMOX overexpression increases muscle fiber size, while SMOX reduction was enough to induce muscle atrophy in multiple murine models. Of note, the SMOX reaction product spermidine appears to be involved in skeletal muscle atrophy/hypertrophy. It is effective in reactivating autophagy, ameliorating the myopathic defects of collagen VI-null mice. Moreover, spermidine treatment, if combined with exercise, can affect D-gal-induced aging-related skeletal muscle atrophy. This review hypothesizes a role for SMOX during skeletal muscle differentiation and outlines its role and that of spermidine in muscle atrophy. The identification of new molecular pathways involved in the maintenance of skeletal muscle health could be beneficial in developing novel therapeutic lead compounds to treat muscle atrophy.
机译：骨骼肌约占总体重的40％。为了抵抗诸如II型糖尿病，心血管疾病和癌症等慢性疾病，保持肌肉健康和功能对于整个身体至关重要。长期缺乏运动，特别是在老年人中，缺乏运动会导致肌肉萎缩，这种病理状态会带来不良后果，例如生活质量差，身体残疾和死亡率高。在鼠骨骼肌C2C12细胞中，在细胞分化过程中发现了精胺氧化酶（SMOX）酶的表达增加。值得注意的是，SMOX的过表达增加了肌肉纤维的大小，而SMOX的减少足以在多个鼠模型中诱发肌肉萎缩。值得注意的是，SMOX反应产物亚精胺似乎与骨骼肌萎缩/肥大有关。它可有效地重新激活自噬，减轻胶原蛋白VI无效小鼠的肌病性缺陷。此外，如果将亚精胺治疗与运动相结合，可能会影响D-gal诱导的衰老相关骨骼肌萎缩。这篇评论假设SMOX在骨骼肌分化过程中的作用，并概述了SMOX和亚精胺在肌肉萎缩中的作用。鉴定涉及维持骨骼肌健康的新分子途径可能有益于开发新型治疗性铅化合物来治疗肌肉萎缩。

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