PDF(Pubmed)
Abstract：
Impaired biomolecules and cellular organelles are gradually built up during the development and aging of organisms, and this deteriorating process is expedited under stress conditions. As a major lysosome-mediated catabolic process, autophagy has evolved to eradicate these damaged cellular components and recycle nutrients to restore cellular homeostasis and fitness. The autophagic activities are altered under various disease conditions such as ischemia-reperfusion cardiac injury, sarcopenia, and genetic myopathies, which impact multiple cellular processes related to cellular growth and survival in cardiac and skeletal muscles. Thus, autophagy has been the focus for therapeutic development to treat these muscle diseases. To develop the specific and effective interventions targeting autophagy, it is essential to understand the molecular mechanisms by which autophagy is altered in heart and skeletal muscle disorders. Herein, we summarize how autophagy alterations are linked to cardiac and skeletal muscle defects and how these alterations occur. We further discuss potential pharmacological and genetic interventions to regulate autophagy activities and their applications in cardiac and skeletal muscle diseases.
摘要：
受损的生物分子和细胞器在生物体的发育和老化过程中逐渐建立起来，在压力条件下，这种恶化的过程会加快。作为一个主要的溶酶体介导的分解代谢过程，自噬已经进化到根除这些受损的细胞成分，并回收营养以恢复细胞稳态和健康。自噬活性在各种疾病条件下发生改变，如缺血再灌注心脏损伤，少肌症,和遗传性肌病,影响与心肌和骨骼肌细胞生长和存活相关的多个细胞过程。因此，自噬一直是治疗这些肌肉疾病的治疗发展的焦点。开发针对自噬的特异性和有效的干预措施，了解心脏和骨骼肌疾病中自噬改变的分子机制至关重要。在这里，我们总结了自噬改变与心肌和骨骼肌缺陷的联系以及这些改变是如何发生的。我们进一步讨论了调节自噬活性的潜在药理和遗传干预措施及其在心脏和骨骼肌疾病中的应用。
