HMGB1 contributes to adriamycin-induced cardiotoxicity via up-regulating autophagy
HMGB1 contributes to adriamycin-induced cardiotoxicity via up-regulating autophagy
复制标题
HMGB1 通过上调自噬导致阿霉素诱导的心脏毒性
DOI：
10.1016/j.toxlet.2018.04.034
复制
发表时间：
2018-08-01
影响因子：
3.5
通讯作者：
He, Qiaojun
中科院分区：
文献类型：
--
作者：
Luo, Peihua;Zhu, Yi;He, Qiaojun
Adriamycin (ADR) is one of the most widely used and effective anthracycline antitumor agents in the treatment of certain hematological malignancies and solid tumors. However, the severe cardiotoxicity of ADR limits its clinical application. So far, the mechanism of the cardiotoxicity of ADR has not been completely clarified. In our research, cardiomyocyte autophagy and cardiac damage were observed in accompany ADR treatment, and autophagy appeared earlier than cardiac damage. Inhibition of autophagy by silencing ATG7 improved the survival rate of cardiomyocytes treated with ADR. The release of HMGB1 increased after ADR treatment, and silencing HMGB1 could reverse cardiomyocyte damage by attenuating autophagy. In addition, the expression of YAP was decreased, and overexpressing YAP down-regulated HMGB1 and alleviated cardiomyocyte damage. These results indicated that autophagy was the leading cause of ADR-induced cardiotoxicity, and HMGB1 played a vital role in the process of up-regulating autophagy.
