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BMB Rep ; 45(9): 489-95, 2012 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23010169

RESUMO

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 CaMKKß 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 CaMKKß), 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.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Isquemia/enzimologia , Quinases Proteína-Quinases Ativadas por AMP , Proteínas Quinases Ativadas por AMP/química , Quinase da Proteína Quinase Dependente de Cálcio-Calmodulina/metabolismo , Glucose/metabolismo , Humanos , Isquemia/patologia , Complexos Multienzimáticos/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Proteínas Serina-Treonina Quinases/metabolismo , Transdução de Sinais
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