Molecular biology of doxorubicin-induced cardiomyopathy

Kód výsledku v 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>

Nalezeny alternativní kódy

RIV/00209805:_____/02:00006206

Výsledek na webu

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DOI - Digital Object Identifier

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Jazyk výsledku

angličtina

Název v původním jazyce

Molecular biology of doxorubicin-induced cardiomyopathy

Popis výsledku v původním jazyce

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

Název v anglickém jazyce

Molecular biology of doxorubicin-induced cardiomyopathy

Popis výsledku anglicky

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

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

EB - Genetika a molekulární biologie

OECD FORD obor

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Projekt

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Návaznosti

Z - Vyzkumny zamer (s odkazem do CEZ)

Rok uplatnění

2002

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Experimental and Clinical Cardiology

ISSN

1202-6626

e-ISSN

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Svazek periodika

1

Číslo periodika v rámci svazku

7

Stát vydavatele periodika

CZ - Česká republika

Počet stran výsledku

5

Strana od-do

35

Kód UT WoS článku

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EID výsledku v databázi Scopus

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