期刊
ONCOTARGET
卷 8, 期 28, 页码 46663-46680出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.16944
关键词
oncocardiology; anthracyclines; heart failure; impaired autophagy and mitophagy; lysosomal dysfunction
资金
- Canadian Institutes for Health Research [FRN-74733]
- Alfred E. Deacon doctoral scholarship, Institute of Cardiovascular Sciences, St. Boniface Hospital Albrechtsen Research Centre
Doxorubicin (Dox) is a cytotoxic drug widely incorporated in various chemotherapy protocols. Severe side effects such as cardiotoxicity, however, limit Dox application. Mechanisms by which Dox promotes cardiac damage and cardiomyocyte cell death have been investigated extensively, but a definitive picture has yet to emerge. Autophagy, regarded generally as a protective mechanism that maintains cell viability by recycling unwanted and damaged cellular constituents, is nevertheless subject to dysregulation having detrimental effects for the cell. Autophagic cell death has been described, and has been proposed to contribute to Dox-cardiotoxicity. Additionally, mitophagy, autophagic removal of damaged mitochondria, is affected by Dox in a manner contributing to toxicity. Here we will review Dox-induced cardiotoxicity and cell death in the broad context of the autophagy and mitophagy processes.
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