Molecular and cellular mechanisms of skeletal muscle atrophy: an update.
Molecular and cellular mechanisms of skeletal muscle atrophy: an update.
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DOI：
10.1007/s13539-012-0074-6
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发表时间：
2012-09
影响因子：
8.9
通讯作者：
Martinet, Wim
中科院分区：
文献类型：
--
作者：
Fanzani, Alessandro;Conraads, Viviane M.;Penna, Fabio;Martinet, Wim
骨骼肌萎缩被定义为肌肉质量减少，当蛋白质降解超过蛋白质合成时就会发生。肌肉萎缩的潜在诱因是长期不动、营养不良、严重烧伤、衰老以及各种严重且通常是慢性的疾病，如慢性心力衰竭、阻塞性肺病、肾衰竭、艾滋病、败血症、免疫紊乱、癌症和营养不良。有趣的是，几种病理生理因素之间的合作，包括不适当的合成代谢（例如，生长激素、胰岛素样生长因子1）和分解代谢蛋白（例如，肿瘤坏死因子α、肌肉生长抑制素），可能会通过激活蛋白酶体和自噬系统或细胞凋亡途径，使平衡向肌肉特异性蛋白质降解倾斜。根据现有文献，我们概述了导致肌肉萎缩的分子和细胞机制。我们还关注目前用于预防肌肉萎缩并阻止其进展的多方面治疗方法。这种方法包括充足的营养支持、运动训练的实施以及可能的药理学化合物。
Skeletal muscle atrophy is defined as a decrease in muscle mass and it occurs when protein degradation exceeds protein synthesis. Potential triggers of muscle wasting are long-term immobilization, malnutrition, severe burns, aging as well as various serious and often chronic diseases, such as chronic heart failure, obstructive lung disease, renal failure, AIDS, sepsis, immune disorders, cancer, and dystrophies. Interestingly, a cooperation between several pathophysiological factors, including inappropriately adapted anabolic (e.g., growth hormone, insulin-like growth factor 1) and catabolic proteins (e.g., tumor necrosis factor alpha, myostatin), may tip the balance towards muscle-specific protein degradation through activation of the proteasomal and autophagic systems or the apoptotic pathway. Based on the current literature, we present an overview of the molecular and cellular mechanisms that contribute to muscle wasting. We also focus on the multifacetted therapeutic approach that is currently employed to prevent the development of muscle wasting and to counteract its progression. This approach includes adequate nutritional support, implementation of exercise training, and possible pharmacological compounds.
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