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Title:
Molecular and cellular mechanisms of anthracycline cardiotoxicity | Cardiovascular Toxicology
Description:
The molecular and cellular mechanisms that cause cumulative dose-dependent anthracycline-cardiotoxicity remain controversial and incompletely understood. Studies examining the effects of anthracyclines in cardiac myocytes in vitro have demonstrated several forms of cellular injury. Cell death in response to anthracyclines can be observed by one of several mechanisms including apoptosis and necrosis. Cell death by apoptosis can be inhibited by dexrazoxane, the iron chelator that is known to prevent clinical development of heart failure at high cumulative anthracycline exposure. Together with clinical evidence for myocyte death after anthracycline exposure, in the form of elevations in serum troponin, make myocyte cell death a probable mechanism for anthracycline-induced cardiac injury. Other mechanisms of myocyte injury include the development of cellular ‘sarcopenia’ characterized by disruption of normal sarcomere structure. Anthracyclines suppress expression of several cardiac transcription factors, and this may play a role in the development of myocyte death as well as sarcopenia. Degradation of the giant myofilament protein titin may represent an important proximal step that leads to accelerated myofilament degradation. Titin is an entropic spring element in the sarcomere that regulates length-dependent calcium sensitivity. Thus titin degradation may lead to impaired diastolic as well as systolic dysfunction, as well as potentiate the effect of suppression of transcription of sarcomere proteins. An interesting interaction has been noted clinically between anthracyclines and newer cancer therapies that target the erbB2 receptor tyrosine kinase. Studies of erbB2 function in viro suggest that signaling through erbB2 by the growth factor neuregulin may regulate cardiac myocyte sarcomere turnover, as well as myocyte-myocyte/myocyte-matrix force coupling. A combination of further in vitro studies, with more careful monitoring of cardiac function after exposure to these cancer therapies, may help to understand to what extent these mechanisms are at work during clinical exposure of the heart to these important pharmaceuticals.
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Topics {✒️}

myocyte-myocyte/myocyte-matrix force coupling month download article/chapter jnk-p38 map kinases d-type cyclin expression i-band protein assemblies cas google scholar anthracycline-induced myofibrillar disarray chee chew lim & douglas superoxide dismutase activity doxorubicin-induced cardiomyocyte apoptosis anthracycline-induced cardiac injury erbb4-dependent activation full article pdf acute lymphoblastic leukemia privacy choices/manage cookies adriamycin-induced cardiotoxicity anthracyclines suppress expression free radical bioogly pi3-kinase/akt rat ventricular myocytes related subjects anthracycline-induced apoptosis cardiac myocyte apoptosis rat cardiac myocytes growth factor neuregulin 145-kilodalton sarcomeric protein normal sarcomere structure doxorubicin-treated children myocyte injury include interleukin-6 induced pi3 myocyte survival pathways doxorubicin-induced apoptosis anthracycline cardiotoxicity published perfused rat heart cellular ‘sarcopenia’ characterized daunorubicin-induced apoptosis drug-induced cardiotoxicity anthracycline-induced cardiomyopathy cardiac transcription factors transient cardiac ischemia cardiac progenitor cells important proximal step anthracycline-induced suppression pi 3k/akt versatile signaling module erbb signaling network myocardial cell hypertrophy gene expression entropic spring element nucleic acid synthesis

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         headline:Molecular and cellular mechanisms of anthracycline cardiotoxicity
         description:The molecular and cellular mechanisms that cause cumulative dose-dependent anthracycline-cardiotoxicity remain controversial and incompletely understood. Studies examining the effects of anthracyclines in cardiac myocytes in vitro have demonstrated several forms of cellular injury. Cell death in response to anthracyclines can be observed by one of several mechanisms including apoptosis and necrosis. Cell death by apoptosis can be inhibited by dexrazoxane, the iron chelator that is known to prevent clinical development of heart failure at high cumulative anthracycline exposure. Together with clinical evidence for myocyte death after anthracycline exposure, in the form of elevations in serum troponin, make myocyte cell death a probable mechanism for anthracycline-induced cardiac injury. Other mechanisms of myocyte injury include the development of cellular ‘sarcopenia’ characterized by disruption of normal sarcomere structure. Anthracyclines suppress expression of several cardiac transcription factors, and this may play a role in the development of myocyte death as well as sarcopenia. Degradation of the giant myofilament protein titin may represent an important proximal step that leads to accelerated myofilament degradation. Titin is an entropic spring element in the sarcomere that regulates length-dependent calcium sensitivity. Thus titin degradation may lead to impaired diastolic as well as systolic dysfunction, as well as potentiate the effect of suppression of transcription of sarcomere proteins. An interesting interaction has been noted clinically between anthracyclines and newer cancer therapies that target the erbB2 receptor tyrosine kinase. Studies of erbB2 function in viro suggest that signaling through erbB2 by the growth factor neuregulin may regulate cardiac myocyte sarcomere turnover, as well as myocyte-myocyte/myocyte-matrix force coupling. A combination of further in vitro studies, with more careful monitoring of cardiac function after exposure to these cancer therapies, may help to understand to what extent these mechanisms are at work during clinical exposure of the heart to these important pharmaceuticals.
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