Muscle atrophy is an inevitable sequel of fasting, denervation, aging, exposure to microgravity, and many human diseases including, cancer, type-2 diabetes, and renal failure. During atrophy the destruction of the muscle's fundamental contractile machinery, the myofibrils, is accelerated leading to a reduction in muscle mass, weakness, frailty, and physical disability. Recent findings indicate that atrophy can be a major cause of death in affected individuals, and inhibition of muscle wasting is likely to prolong survival. Major advances in our understanding of the mechanisms for myofibril breakdown in atrophy include the discovery of biological pathways and key components that play prominent roles. On fasting or denervation, degradation of myofibrillar proteins requires an initial dissociation of the desmin cytoskeleton, whose integrity is critical for myofibril stability. This loss of desmin filaments involves phosphorylation, ubiquitination, and subsequent depolymerization by calpain-1, and appears to reduce myofibrils integrity and facilitate their destruction. Consequently, depolymerization of desmin filament in atrophy seems to be an early key event for overall proteolysis. A focus of this review is to discuss these new insights and the specific role of calpain-1 in promoting desmin filaments loss, and to highlight important key questions that merit further study.

肌肉萎缩是禁食，神经支配，衰老，暴露于微重力以及许多人类疾病（包括癌症，2型糖尿病和肾衰竭）的必然结果。在萎缩期间，肌肉的基本收缩机制肌原纤维的破坏加速，导致肌肉质量，无力，虚弱和身体残疾的减少。最近的发现表明，萎缩可能是受影响个体死亡的主要原因，抑制肌肉消瘦可能会延长生存期。我们对肌萎缩中肌原纤维分解机制的理解的主要进展包括发现了起重要作用的生物途径和关键成分。禁食或去神经支配时，肌原纤维蛋白的降解需要初次分离结蛋白细胞骨架，其完整性对肌原纤维的稳定性至关重要。结蛋白细丝的这种损失包括磷酸化，泛素化和随后的钙蛋白酶1解聚，似乎降低了肌原纤维的完整性并促进了其破坏。因此，萎缩性结节纤丝的解聚似乎是整体蛋白水解的早期关键事件。这篇综述的重点是讨论这些新的见解以及calpain-1在促进结蛋白丝损失方面的具体作用，并重点突出值得进一步研究的重要关键问题。萎缩性结节纤丝的解聚似乎是整体蛋白水解的早期关键事件。这篇综述的重点是讨论这些新的见解以及钙蛋白酶-1在促进结蛋白丝损失方面的特定作用，并重点突出值得进一步研究的重要关键问题。萎缩性结节纤丝的解聚似乎是整体蛋白水解的早期关键事件。这篇综述的重点是讨论这些新的见解以及calpain-1在促进结蛋白丝损失方面的具体作用，并重点突出值得进一步研究的重要关键问题。