Molecular biology of doxorubicin-induced cardiomyopathy

Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14330%2F02%3A00007255" target="_blank" >RIV/00216224:14330/02:00007255 - isvavai.cz</a>
Alternative codes found
RIV/00209805:_____/02:00006206
Result on the web
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DOI - Digital Object Identifier
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Result language
angličtina
Original language name
Molecular biology of doxorubicin-induced cardiomyopathy
Original language description
A severe, cumulative, dose-dependent chronic cardiac toxicity is the major limitation of anthracycline therapy. Chronic cardiotoxicity occurs in patients after prolonged administration of Dox; a similar cardiotoxicity can be elicited in many animal species, including the mouse, the rat, the rabbit, the dog , and the monkey, after treatment with Dox. The cardiotoxicity consists of a chronic, progressive cardiomyopathy with myocyte vacuolation and degeneration, interstitial edema, and fibroplasia leadingto congestive haert failure. Despite considerable work on the subject, the pathogenesis of the doxorubicin-induced cardiomyopathy is not well understood. However, Dox has been shown to exert a multiplicity of complex biochemical effects on the myocardium, including the following: binding to DNA and alteration of nucleic acids and protein synthesis, lipid peroxidation subsequent to free radical generation, release of histamine and catecholamines, damage to mitochondria, an effect on vario
Czech name
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Czech description
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Type
J<sub>x</sub> - Unclassified - Peer-reviewed scientific article (Jimp, Jsc and Jost)
CEP classification
EB - Genetics and molecular biology
OECD FORD branch
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Publication year
2002
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

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