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AMP-activated protein kinase: implications on ischemic diseases

Authors
Ahn, Yong-JooKim, HwewonLim, HeejinLee, MaxKang, YuhyunMoon, SangJunKim, Hyeon SooKim, Hyung-Hwan
Issue Date
30-Sep-2012
Publisher
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
Keywords
AMPK; CaMKK beta; Ischemia; LKBI
Citation
BMB REPORTS, v.45, no.9, pp.489 - 495
Indexed
SCIE
SCOPUS
KCI
Journal Title
BMB REPORTS
Volume
45
Number
9
Start Page
489
End Page
495
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/107426
DOI
10.5483/BMBRep.2012.45.9.169
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 due to ischemia, stresses, such as the disruption of blood glucose homeostasis, hypoglycemia and hypoxia, activate the AMPK complex. LKB1 and CaMKK beta 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 CaMKK beta), 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. [BMB Reports 2012; 45(9): 489-495]
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