Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account

被引:12
|
作者
Vitale, Roberta [1 ]
Marzocco, Stefania [1 ]
Popolo, Ada [1 ]
机构
[1] Univ Salerno, Dept Pharm, I-84084 Fisciano, Italy
关键词
cardiotoxicity; Doxorubicin; oxidative stress; inflammation; NITRIC-OXIDE; DRUG-DELIVERY; ANTHRACYCLINE CARDIOTOXICITY; INDUCED CARDIOMYOPATHY; CARDIAC DYSFUNCTION; PANAX-GINSENG; CARVEDILOL; NRF2; ANTIOXIDANT; MECHANISMS;
D O I
10.3390/ijms25137477
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cardiotoxicity is the main side effect of several chemotherapeutic drugs. Doxorubicin (Doxo) is one of the most used anthracyclines in the treatment of many tumors, but the development of acute and chronic cardiotoxicity limits its clinical usefulness. Different studies focused only on the effects of long-term Doxo administration, but recent data show that cardiomyocyte damage is an early event induced by Doxo after a single administration that can be followed by progressive functional decline, leading to overt heart failure. The knowledge of molecular mechanisms involved in the early stage of Doxo-induced cardiotoxicity is of paramount importance to treating and/or preventing it. This review aims to illustrate several mechanisms thought to underlie Doxo-induced cardiotoxicity, such as oxidative and nitrosative stress, inflammation, and mitochondrial dysfunction. Moreover, here we report data from both in vitro and in vivo studies indicating new therapeutic strategies to prevent Doxo-induced cardiotoxicity.
引用
收藏
页数:20
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