Molecular biology of doxorubicin-induced cardiomyopathy

J 2002

Molecular biology of doxorubicin-induced cardiomyopathy

UMLAUF, Jozef a Marcel HORKÝ

Základní údaje

Originální název

Molecular biology of doxorubicin-induced cardiomyopathy

Autoři

UMLAUF, Jozef a Marcel HORKÝ

Vydání

Experimental and Clinical Cardiology, Canada, Pulsus Group Inc. 2002, 1202-6626

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

Genetika a molekulární biologie

Stát vydavatele

Česká republika

Utajení

není předmětem státního či obchodního tajemství

Kód RIV

RIV/00216224:14330/02:00007255

Organizační jednotka

Fakulta informatiky

Klíčová slova anglicky

doxorubicin; cardiomyopathy; DNA damage; mitochondrial dysfunction; cardioprotection

Štítky

cardiomyopathy, cardioprotection, DNA damage, doxorubicin, mitochondrial dysfunction

Změněno: 31. 5. 2003 10:15, RNDr. JUDr. Vladimír Šmíd, CSc.

Anotace

V originále

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.

Návaznosti

MSM 141100002, záměr

Název: Molekulární patofyziologie multigenních chorob

Investor: Ministerstvo školství, mládeže a tělovýchovy ČR, Molekulární patofyziologie multigenních chorob

Citovat

UMLAUF, Jozef a Marcel HORKÝ. Molecular biology of doxorubicin-induced cardiomyopathy. Experimental and Clinical Cardiology. Canada: Pulsus Group Inc., 2002, roč. 1, č. 7, s. 35-39. ISSN 1202-6626.

@article{483368,
   author = {Umlauf, Jozef and Horký, Marcel},
   article_location = {Canada},
   article_number = {7},
   keywords = {doxorubicin; cardiomyopathy; DNA damage; mitochondrial dysfunction; cardioprotection},
   language = {eng},
   issn = {1202-6626},
   journal = {Experimental and Clinical Cardiology},
   title = {Molecular biology of doxorubicin-induced cardiomyopathy},
   volume = {1},
   year = {2002}
}

TY  - JOUR
ID  - 483368
AU  - Umlauf, Jozef - Horký, Marcel
PY  - 2002
TI  - Molecular biology of doxorubicin-induced cardiomyopathy
JF  - Experimental and Clinical Cardiology
VL  - 1
IS  - 7
SP  - 35
EP  - 35
PB  - Pulsus Group Inc.
SN  - 12026626
KW  - doxorubicin
KW  - cardiomyopathy
KW  - DNA damage
KW  - mitochondrial dysfunction
KW  - cardioprotection
N2  - 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.
ER  -

UMLAUF, Jozef a Marcel HORKÝ. Molecular biology of doxorubicin-induced cardiomyopathy. \textit{Experimental and Clinical Cardiology}. Canada: Pulsus Group Inc., 2002, roč.~1, č.~7, s.~35-39. ISSN~1202-6626.

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