Autophagy in striated muscle diseases.
Autophagy in striated muscle diseases.
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DOI：
10.3389/fcvm.2022.1000067
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发表时间：
2022
影响因子：
3.6
通讯作者：
中科院分区：
文献类型：
--
作者：
受损的生物分子和细胞器在生物体的发育和衰老过程中逐渐建立，并且这种退化过程在应激条件下加速。自噬作为一种主要的溶酶体介导的分解代谢过程，已经进化为清除这些受损的细胞组分并回收营养以恢复细胞内稳态和适应性。自噬活性在各种疾病条件下改变，例如缺血-再灌注心脏损伤、肌肉减少症和遗传性肌病，其影响与心脏和骨骼肌中的细胞生长和存活相关的多个细胞过程。因此，自噬已经成为治疗这些肌肉疾病的治疗开发的焦点。为了开发针对自噬的特异性和有效的干预措施，有必要了解心脏和骨骼肌疾病中自噬改变的分子机制。在此，我们总结了自噬改变如何与心脏和骨骼肌缺陷有关，以及这些改变如何发生。我们进一步讨论了潜在的药理学和遗传干预，以调节自噬活动及其在心脏和骨骼肌疾病中的应用。
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.
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