UMLAUF, Jozef and Marcel HORKÝ. Molecular biology of doxorubicin-induced cardiomyopathy. Experimental and Clinical Cardiology. Canada: Pulsus Group Inc., 2002, vol. 1, No 7, p. 35-39. ISSN 1202-6626.
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Basic information
Original name Molecular biology of doxorubicin-induced cardiomyopathy
Authors UMLAUF, Jozef (203 Czech Republic, guarantor) and Marcel HORKÝ (203 Czech Republic).
Edition Experimental and Clinical Cardiology, Canada, Pulsus Group Inc. 2002, 1202-6626.
Other information
Original language English
Type of outcome Article in a journal
Field of Study Genetics and molecular biology
Country of publisher Czech Republic
Confidentiality degree is not subject to a state or trade secret
RIV identification code RIV/00216224:14330/02:00007255
Organization unit Faculty of Informatics
Keywords in English doxorubicin; cardiomyopathy; DNA damage; mitochondrial dysfunction; cardioprotection
Tags cardiomyopathy, cardioprotection, DNA damage, doxorubicin, mitochondrial dysfunction
Changed by Changed by: RNDr. JUDr. Vladimír Šmíd, CSc., učo 1084. Changed: 31/5/2003 10:15.
Abstract
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 leading to 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 various cellular membranes, an excess calcium influx, and an effect on collagen matrix. A combination of these effects probably triggers the myocardial lesion.
Links
MSM 141100002, plan (intention)Name: Molekulární patofyziologie multigenních chorob
Investor: Ministry of Education, Youth and Sports of the CR, Molecular pathophysiology of multigene diseases
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