Adriamycin-induced heart failure: mechanisms and modulation

Adriamycin-induced heart failure: mechanisms and modulation
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DOI:
10.1023/a:1007094214460
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发表时间:
2000-04-01
影响因子:
4.3
通讯作者:
Iliskovic, N
Iliskovic, N
中科院分区:
生物学3区
文献类型:
--
作者:
Singal, P;Li, TM;Iliskovic, N

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阿霉素(阿霉素)是针对多种癌症最有效的化疗药物之一,但其用途因发生心力衰竭的风险而严重削弱。现有的实验室证据表明,自由基产生增加和心肌内源性抗氧化剂减少导致氧化应激增加,在心力衰竭的发病机制中起着重要作用。阿霉素诱导的细胞凋亡和高脂血症也可能参与该过程。普罗布考是一种降脂药和抗氧化剂,通过减少氧化应激以及调节细胞凋亡和高脂质浓度来完全预防心力衰竭的发生。因此,阿霉素和普罗布考的联合治疗对于优化癌症患者的治疗具有很大的潜力。
Adriamycin (doxorubicin) is one of the most effective chemotherapeutic agents against a variety of cancers, but its usefulness is seriously curtailed by the risk of developing heart failure. Available laboratory evidence suggests that an increase in oxidative stress, brought about by increased free radical production and decreased myocardial endogenous antioxidants, plays an important role in the pathogenesis of heart failure. Adriamycin-induced apoptosis and hyperlipidemia may also be involved in the process. Probucol, a lipid-lowering drug and an antioxidant, completely prevents the occurrence of heart failure by reducing oxidative stress as well as by the modulation of apoptis and high lipid concentrations. Thus, combined therapy with adriamycin and probucol has a high potential for optimizing the treatment of cancer patients.