Cardiomyocyte death in doxorubicin-induced cardiotoxicity

Content Provider	Semantic Scholar
Author	Zhang, Yingyuan Shi, Jianjian Li, Yuan-Jian
Copyright Year	2009
Abstract	Doxorubicin (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.
Starting Page	435
Ending Page	445
Page Count	11
File Format	PDF HTM / HTML
DOI	10.1007/s00005-009-0051-8
PubMed reference number	19866340
Journal	Medline
Volume Number	57
Alternate Webpage(s)	https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC2809808&blobtype=pdf
Alternate Webpage(s)	https://doi.org/10.1007/s00005-009-0051-8
Journal	Archivum Immunologiae et Therapiae Experimentalis
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article