期刊
CELL BIOCHEMISTRY AND BIOPHYSICS
卷 60, 期 3, 页码 311-322出版社
HUMANA PRESS INC
DOI: 10.1007/s12013-011-9153-0
关键词
Doxorubicin; Myocardial toxicity; AMPK; JNK; p53; mTORC1
资金
- Natural Science Foundation of Jiangsu Province [BK2010160]
Despite its potent antitumor effect, clinical use of Doxorubicin is limited because of serious side effects including myocardial toxicity. Understanding the cellular mechanism involved in this process in a better manner is beneficial for optimizing Doxorubicin treatment. In the current study, the authors focus on the AMP-activated protein kinase (AMPK) in the said process. In this study, the authors discovered for the first time that Doxorubicin induces AMPK activation in cultured rat embryonic ventricular myocardial H9c2 cells. Reactive oxygen species (ROS)-dependent LKB1 activation serves as the upstream signal for AMPK activation by Doxorubicin. Evidence in support of the activation of AMPK contributing to Doxorubicin-induced H9c2 cell death/apoptosis-probably by modulating multiple downstream signal targets, including regulating JNK, p53, and inhibiting mTORC1-is provided in this article.
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