Health & Environmental Research Online (HERO)


Print Feedback Export to File
1560378 
Journal Article 
Doxorubicin-induced cardiomyopathy: From molecular mechanisms to therapeutic strategies 
Octavia, Y; Tocchetti, CG; Gabrielson, KL; Janssens, S; Crijns, HJ; Moens, AnL 
2012 
Yes 
Journal of Molecular and Cellular Cardiology
ISSN: 0022-2828
EISSN: 1095-8584 
52 
6 
1213-1225 
22465037 
WOS:000304227200002 
The utility of anthracycline antineoplastic agents in the
clinic is compromised by the risk of cardiotoxicity. It has been calculated that approximately
10% of patients treated with doxorubicin or its derivatives will develop cardiac complications up
to 10 years after the cessation of chemotherapy. Oxidative stress has been established as the
primary cause of cardiotoxicity. However, interventions reducing oxidative stress have not been
successful at reducing the incidence of cardiotoxicity in patients treated with doxorubicin. New
insights into the cardiomyocyte response to oxidative stress demonstrate that underlying
differences between in vitro and in vivo toxicities may modulate the response to superoxide
radicals and related compounds. This has led to potentially new uses for pre-existing drugs and
new avenues of exploration to find better pharmacotherapies and interventions for the prevention
of cardiotoxicity. However, much work still must be done to validate the clinical utility of
these new approaches and proposed mechanisms. In this review, the authors have reviewed the
molecular mechanisms of the pathogenesis of acute and chronic doxorubicin-induced cardiotoxicity
and propose potential pharmacological interventions and treatment options to prevent or reverse
this specific type of heart failure. (C) 2012 Elsevier Ltd. All rights reserved. 
Doxorubicin; Anthracyclines; Cardiotoxicity; Heart failure; Oxidative stress; Cardioprotection