多柔比星诱导的骨骼肌功能障碍机制研究进展

Research advances in mechanism of doxorubicin-induced skeletal muscle dysfunction

多柔比星(DOX)作为广谱抗肿瘤药物,临床中用于多种癌症的治疗。然而,DOX在使用时可剂量依赖性诱导骨骼肌功能障碍,致使癌症患者生存质量明显下降。本文通过对DOX毒性作用、DOX诱导骨骼肌功能障碍特点以及DOX诱导骨骼肌功能障碍的相关发生机制进行综述,重点对氧化应激、Ca2+超载、线粒体能量代谢失调、细胞自噬与凋亡、一氧化氮浓度和氨基酸代谢及肌源性调节因子表达等病理机制进行总结,并对未来研究方向予以展望,希望为临床深入研究DOX肌肉毒性作用提供理论依据。

Doxorubicin(DOX)is a widely used clinical anti-tumor drug for cancer.Unfortunately,DOX can also cause skeletal muscle dysfunction in a dose-dependent manner,leading to a significant decline in the quality of life of cancer patients.In this paper,we summarize the toxic effects of DOX,the characteristics of DOX-induced skeletal muscle dysfunction and its related mechanisms.We focus on pathological mechanisms,including oxidative stress,Ca2+overload,mitochondrial energy metabolism disorder,autophagy and apoptosis,nitric oxide concentration and amino acid metabolism and myogenic regulatory factor expression.Research prospects are outlined.It is expected to provide a theoretical basis for the clinical study of DOX toxicity.