NDLI: Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

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Activation of AMP-Activated Protein Kinase Contributes to Doxorubicin-Induced Cell Death and Apoptosis in Cultured Myocardial H9c2 Cells

Content Provider	Springer Nature Link
Author	Chen, Min Bin Wu, Xiao Yang Gu, Jin Hua Guo, Qing Tao Shen, Wen Xiang Lu, Pei Hua
Copyright Year	2011
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.
Starting Page	311
Ending Page	322
Page Count	12
File Format	PDF
ISSN	10859195
Journal	Cell Biochemistry and Biophysics
Volume Number	60
Issue Number	3
e-ISSN	15590283
Language	English
Publisher	Humana Press Inc
Publisher Date	2011-01-28
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Doxorubicin Myocardial toxicity AMPK JNK p53 mTORC1 Biophysics and Biological Physics Pharmacology/Toxicology Biochemistry Cell Biology Biotechnology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Medicine Biochemistry Biophysics

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