Stress signaling in the heart by AMP-activated protein kinase

被引:0
|
作者
Raymond Russell
机构
[1] Yale University School of Medicine,Section of Cardiovascular Medicine
来源
关键词
Human Umbilical Vein Endothelial Cell; Fatty Acid Oxidation; AICAR; Increase Glucose Uptake; Thr172 Phosphorylation;
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摘要
The stress-signaling protein, adenosine monophosphate-activated protein kinase (AMPK), regulates a variety of pathways in cells that 1) increase the provision and utilization of energy-providing substrates such as glucose and fatty acids, 2) inhibit energy-requiring pathways such as cholesterol biosynthesis and protein synthesis, and 3) increase the transcription of genes involved in energy metabolism and mitochondrial biogenesis. In the heart, AMPK therefore becomes very important in protecting against ischemia-reperfusion injury and regulating substrate metabolism in the face of changes in workload. This review summarizes the regulation of AMPK activity in the heart and discusses the effects of AMPK activation.
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页码:446 / 450
页数:4
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