Document Detail


AMP-activated protein kinase, stress responses and cardiovascular diseases.
MedLine Citation:
PMID:  22390198     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AMPK (AMP-activated protein kinase) is one of the key players in maintaining intracellular homoeostasis. AMPK is well known as an energy sensor and can be activated by increased intracellular AMP levels. Generally, the activation of AMPK turns on catabolic pathways that generate ATP, while inhibiting cell proliferation and biosynthetic processes that consume ATP. In recent years, intensive investigations on the regulation and the function of AMPK indicates that AMPK not only functions as an intracellular energy sensor and regulator, but is also a general stress sensor that is important in maintaining intracellular homoeostasis during many kinds of stress challenges. In the present paper, we will review recent literature showing that AMPK functions far beyond its proposed energy sensor and regulator function. AMPK regulates ROS (reactive oxygen species)/redox balance, autophagy, cell proliferation, cell apoptosis, cellular polarity, mitochondrial function and genotoxic response, either directly or indirectly via numerous downstream pathways under physiological and pathological conditions.
Authors:
Shaobin Wang; Ping Song; Ming-Hui Zou
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  122     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-03-06     Completed Date:  2012-04-30     Revised Date:  2013-04-01    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  555-73     Citation Subset:  IM    
Affiliation:
Section of Molecular Medicine, University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA.
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / physiology*
Animals
Anoxia
Antioxidants / metabolism
Autophagy
Cardiovascular Diseases / metabolism
Cell Proliferation
Gene Expression Regulation
Humans
Metformin / metabolism
Mice
Mitochondria / metabolism
Models, Biological
NADPH Oxidase / metabolism
Oxidation-Reduction
Reactive Oxygen Species
Grant Support
ID/Acronym/Agency:
R01 HL074399/HL/NHLBI NIH HHS; R01 HL079584/HL/NHLBI NIH HHS; R01 HL080499/HL/NHLBI NIH HHS; R01 HL089920/HL/NHLBI NIH HHS; R01 HL096032/HL/NHLBI NIH HHS; R01 HL105157/HL/NHLBI NIH HHS; R01 HL110488/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 657-24-9/Metformin; EC 1.6.3.1/NADPH Oxidase; EC 2.7.11.1/AMP-Activated Protein Kinases
Comments/Corrections

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