Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells |
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Authors: | Min-Bin Chen Xiao-Yang Wu Jin-Hua Gu Qing-Tao Guo Wen-Xiang Shen Pei-Hua Lu |
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Institution: | (1) Department of Medical Oncology, Kunshan First People’s Hospital Affiliated to Jiangsu University, 91 Qianjin Road, Kunshan, 215300, Jiangsu Province, China;(2) Department of Gastrointestinal Surgery, Kunshan First People’s Hospital Affiliated to Jiangsu University, 91 Qianjin Road, Kunshan, 215300, Jiangsu Province, China;(3) Department of Medical Laboratory Center, Kunshan First People’s Hospital Affiliated to Jiangsu University, 91 Qianjin Road, Kunshan, 215300, Jiangsu Province, China;(4) Department of Surgery, Wuxi People’s Hospital of Nanjing Medical University, 299 Qingyang Road, Wuxi City, 214000, Jiangsu Province, China |
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Abstract: | 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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