2001
DOI: 10.1016/s0014-2999(01)00765-8
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Doxorubicin and mechanical performance of cardiac trabeculae after acute and chronic treatment: a review

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Cited by 156 publications
(108 citation statements)
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“…The cardiotoxic effects of doxorubicin have been extensively investigated. The effects on mechanical performance of the heart have been described; a variety of pathogenetic mechanisms have also been elucidated (including mitochondrial dysfunction, free radical production, changes in iron handling) and the cellular and molecular mechanisms of the myocyte apoptosis and necrosis have been characterized in much detail overviewed in [3][4][5][6]. Recent work demonstrated the close relationship between oxidative and nitrosative stress and PARP activation in doxorubicin-treated animals as well as in humans undergoing doxorubicin anticancer therapy [7][8][9].…”
Section: Introductionmentioning
confidence: 99%
“…The cardiotoxic effects of doxorubicin have been extensively investigated. The effects on mechanical performance of the heart have been described; a variety of pathogenetic mechanisms have also been elucidated (including mitochondrial dysfunction, free radical production, changes in iron handling) and the cellular and molecular mechanisms of the myocyte apoptosis and necrosis have been characterized in much detail overviewed in [3][4][5][6]. Recent work demonstrated the close relationship between oxidative and nitrosative stress and PARP activation in doxorubicin-treated animals as well as in humans undergoing doxorubicin anticancer therapy [7][8][9].…”
Section: Introductionmentioning
confidence: 99%
“…However, its utility is limited by DOX-induced cardiotoxicity, mainly due to free radical induced myocardial injury, lipid peroxidation, mitochondrial damage and cellular toxicity (De Beer et al, 2001;In Duk et al, 2002;Li et al, 2007;Kanu et al, 2010;Verma and Vinayak, 2012;Vishwanatha et al, 2012). Several researchers have reported that an organism is generally protected from damage caused by free radicals by means of its antioxidant defence system.…”
Section: Introductionmentioning
confidence: 99%
“…(3) inhibition of cardiac specific muscle gene transcription and translation, in combination with an increase in myofibril protein degradation, leading to loss of myofibrils (Lewis and Gonzalez, 1987;Ito et al, 1990;Kurabayashi et al, 1994;Toyoda et al, 1998;d'Anglemont de Tassigny et al, 2004;Lim et al, 2004b), and (4) disturbance of intracellular calcium homeostasis (De Beer et al, 2001;Wallace, 2003). The mechanism of doxorubicin-induced free radical generation and oxidative stress has been reviewed in other chapters of this book as well as comprehensive reviews in the field (Singal et al, 2000;Berthiaume and Wallace, 2007;Simunek et al, 2009).…”
mentioning
confidence: 99%