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Cardiomyocyte death in doxorubicin-induced cardiotoxicity Zhang YW; Shi J; Li YJ; Wei LArch Immunol Ther Exp (Warsz) 2009[Nov]; 57 (6): 435-45Doxorubicin (DOX) is one of the most widely used and successful antitumor drugs, but its cumulative and dose-dependent cardiac toxicity has been a major concern of oncologists in cancer therapeutic practice for decades. With the increasing population of cancer survivors, there is a growing need to develop preventive strategies and effective therapies against DOX-induced cardiotoxicity, in particular late-onset cardiomyopathy. Although intensive investigations on DOX-induced cardiotoxicity have continued for decades, the underlying mechanisms responsible for DOX-induced cardiotoxicity have not been completely elucidated. A rapidly expanding body of evidence supports the notion that cardiomyocyte death by apoptosis and necrosis is a primary mechanism of DOX-induced cardiomyopathy and that other types of cell death, such as autophagy and senescence/aging, may participate in this process. This review focuses on the current understanding of the molecular mechanisms underlying DOX-induced cardiomyocyte death, including the major primary mechanism of excess production of reactive oxygen species (ROS) and other recently discovered ROS-independent mechanisms. The different sensitivities to DOX-induced cell death signals between adult and young cardiomyocytes will also be discussed.|Animals[MESH]|Cardiomyopathies/*chemically induced/prevention & control[MESH]|Cardiotoxins/*adverse effects/therapeutic use[MESH]|Cell Death/drug effects[MESH]|Cellular Senescence[MESH]|Doxorubicin/*adverse effects/therapeutic use[MESH]|Humans[MESH]|Myocytes, Cardiac/drug effects/pathology[MESH]|Neoplasms/*drug therapy[MESH]|Reactive Oxygen Species[MESH] |
