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本文引用的文献

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American Society of Clinical Oncology clinical practice guidelines for the use of chemotherapy and radiotherapy protectants.美国临床肿瘤学会关于化疗和放疗保护剂使用的临床实践指南。
J Clin Oncol. 1999 Oct;17(10):3333-55. doi: 10.1200/JCO.1999.17.10.3333.
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Protective effects of carvedilol against doxorubicin-induced cardiomyopathy in rats.卡维地洛对阿霉素诱导的大鼠心肌病的保护作用。
Life Sci. 1999;65(12):1265-74. doi: 10.1016/s0024-3205(99)00362-8.
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Adriamycin-induced changes of creatine kinase activity in vivo and in cardiomyocyte culture.
Toxicology. 1999 May 3;134(1):51-62. doi: 10.1016/s0300-483x(99)00039-6.
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Zinc accumulation in adriamycin-induced cardiomyopathy in rats: effects of melatonin, a cardioprotective antioxidant.锌在阿霉素诱导的大鼠心肌病中的蓄积：心脏保护抗氧化剂褪黑素的作用
J Pineal Res. 1999 May;26(4):204-10. doi: 10.1111/j.1600-079x.1999.tb00585.x.
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A calcium antagonist protects against doxorubicin-induced impairment of calcium handling in neonatal rat cardiac myocytes.一种钙拮抗剂可防止阿霉素诱导的新生大鼠心肌细胞钙处理功能受损。
Jpn Circ J. 1999 Feb;63(2):123-9. doi: 10.1253/jcj.63.123.
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TAFII250, Egr-1, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin.阿霉素处理的小鼠和新生大鼠心肌细胞中TAFII250、Egr-1和D型细胞周期蛋白的表达
Am J Physiol. 1999 Mar;276(3):H803-14. doi: 10.1152/ajpheart.1999.276.3.H803.
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In vivo prevention of adriamycin cardiotoxicity by cyclosporin A or FK506.环孢素A或FK506对阿霉素心脏毒性的体内预防作用
Toxicology. 1998 Nov 16;131(2-3):175-81. doi: 10.1016/s0300-483x(98)00128-0.
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Doxorubicin cardiotoxicity: diastolic cardiac myocyte dysfunction as a result of impaired calcium handling in isolated cardiac myocytes.阿霉素心脏毒性：在分离的心肌细胞中，由于钙处理受损导致舒张期心肌细胞功能障碍。
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Sarcoplasmic reticulum genes are selectively down-regulated in cardiomyopathy produced by doxorubicin in rabbits.在阿霉素诱导的兔心肌病中，肌浆网基因被选择性下调。
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Use of cardiac troponin T levels as an indicator of doxorubicin-induced cardiotoxicity.使用心肌肌钙蛋白T水平作为多柔比星诱导的心脏毒性的指标。
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阿霉素诱导的心肌病的分子生物学

Molecular biology of doxorubicin-induced cardiomyopathy.

作者信息

Umlauf J, Horký M

机构信息

Masaryk Memorial Cancer Institute and.

出版信息

Exp Clin Cardiol. 2002 Spring;7(1):35-9.

PMID:19644577
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2716188/
Abstract

The anthracycline doxorubicin is an antineoplastic agent, eliciting chronic cardiac toxicity. It occurs in patients after prolonged administration of doxorubicin, leading to congestive heart failure. The pathogenesis of the doxorubicin-induced car-diomyopathy is not well understood. The present article summarizes the unique effect of doxorubicin on cardiac-specific gene expression. In addition to binding to DNA, doxorubicin directly affects the function of a variety of proteins. Free radical generation, damage to mitochondria and active cell death are also critical in the development of doxorubicin-induced cardiac toxicity. Agents providing effective cardioprotection are also reviewed.

摘要

蒽环类药物阿霉素是一种抗肿瘤药，会引发慢性心脏毒性。它发生在长期使用阿霉素的患者身上，可导致充血性心力衰竭。阿霉素诱导的心肌病的发病机制尚不完全清楚。本文总结了阿霉素对心脏特异性基因表达的独特作用。除了与DNA结合外，阿霉素还直接影响多种蛋白质的功能。自由基生成、线粒体损伤和细胞主动死亡在阿霉素诱导的心脏毒性发展中也起关键作用。本文还综述了提供有效心脏保护作用的药物。