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AMP-activated protein kinase: implications on ischemic diseases

Title
AMP-activated protein kinase: implications on ischemic diseases
Author(s)
Ahn, Yong-JooKim, HwewonLim, HeejinLee, MaxKang, YuhyunMoon, SangJunKim, Hyeon SooKim, Hyung-Hwan
DGIST Authors
Moon, SangJun
Issued Date
2012-09
Type
Article
Article Type
Review
Author Keywords
AMPKCaMKK betaIschemiaLKBI
Keywords
NITRIC-OXIDE SYNTHASEENDOTHELIAL-CELLSUPSTREAM KINASESKELETAL-MUSCLEBETAANGIOGENESISADIPONECTININHIBITIONMETFORMINBINDING
ISSN
1976-6696
Abstract
Ischemia is a blockage of blood supply due to an embolism or a hemorrhage in a blood vessel. When an organ cannot receive oxygenated blood and can therefore no longer replenish its blood supply dueto ischemia, stresses, such as the disruption of blood glucose homeostasis, hypoglycemia and hypoxia, activate the AMPK complex. LKB1 and CaMKKβ are essential activators of the AMPK signaling pathway. AMPK triggers proangiogenic effects through the eNOS protein in tissues with ischemic conditions, where cells are vulnerable to apoptosis, autophagy and necrosis. The AMPK complex acts to restore blood glucose levels and ATP levels back to homeostasis. This review will discuss AMPK, as well as its key activators (LKB1 and CaMKKβ), as a central energy regulator and evaluate the upstream and downstream regulating pathways of AMPK. We will also discuss how we can control this important enzyme in ischemic conditions to prevent harmful effects in patients with vascular damage. © 2012 by the The Korean Society for Biochemistry and Molecular Biology.
URI
http://hdl.handle.net/20.500.11750/2457
DOI
10.5483/BMBRep.2012.45.9.169
Publisher
Korean Society for Molecular and Cellular Biology

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