摘要
Abstract
Doxorubicin (DOX) is one of the most widely used and successful antitumor drugs.The major side effect of DOX treatment is cumulative, dose-dependent cardiac toxicity and irreversible myocardial damage which results in refractory congestive heart failure (CHF). A rapidly growing evidence supports that cardiomyocyte death by apoptosis and necrosis is a primary mechanism for DOX-induced cardiomyopathy. Other types of cell death, such as autophagy and senescence/aging, may participate in this process, too. In this review, we focused on the current understanding of molecular mechanisms underlying DOX-induced cardiomyocyte death, including the excess production of reactive oxygen species (ROS), subsequent dysregulation of calcium homeostasis, mitochondrial damage, DNA lesions,activation of transcription factors, and so on. In addition, ROS-independent mechanisms are also thought to take partial responsibility for DOX-induced cardiomyocyte death. The potential strategies to reduce DOX-induced cardiomyocyte death were also discussed.关键词
阿霉素/心肌病变/细胞凋亡/细胞坏死/自我吞噬Key words
doxorubicin/ cardiomyopathy/ apoptosis/ necrosis/ autophagy
