| AMP-activated protein kinase, stress responses and cardiovascular diseases. | |
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MedLine Citation:
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PMID: 22390198 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Shaobin Wang; Ping Song; Ming-Hui Zou |
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Publication Detail:
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Type: Journal Article; Review |
Journal Detail:
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Title: Clinical science (London, England : 1979) Volume: 122 ISSN: 1470-8736 ISO Abbreviation: Clin. Sci. Publication Date: 2012 Jun |
Date Detail:
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Created Date: 2012-03-06 Completed Date: 2012-04-30 Revised Date: 2013-04-01 |
Medline Journal Info:
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Nlm Unique ID: 7905731 Medline TA: Clin Sci (Lond) Country: England |
Other Details:
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Languages: eng Pagination: 555-73 Citation Subset: IM |
Affiliation:
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Section of Molecular Medicine, University of Oklahoma Health Science Center, Oklahoma City, OK 73104, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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AMP-Activated Protein Kinases
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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:
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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:
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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 | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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