作者: Min-Bin Chen , Xiao-Yang Wu , Jin-Hua Gu , Qing-Tao Guo , Wen-Xiang Shen
DOI: 10.1007/S12013-011-9153-0
关键词:
摘要: Despite its potent antitumor effect, clinical use of Doxorubicin is limited because serious side effects including myocardial toxicity. Understanding the cellular mechanism involved in this process a better manner beneficial for optimizing treatment. In current study, authors focus on AMP-activated protein kinase (AMPK) said process. discovered first time that induces AMPK activation cultured rat embryonic ventricular H9c2 cells. Reactive oxygen species (ROS)-dependent LKB1 serves as upstream signal by Doxorubicin. Evidence support contributing to Doxorubicin-induced cell death/apoptosis—probably modulating multiple downstream targets, regulating JNK, p53, and inhibiting mTORC1—is provided article.