| Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation. | |
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MedLine Citation:
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PMID: 21552292 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Aim:To identify the role of metformin in cardiac hypertrophy and investigate the possible mechanism underlying this effect.Methods:Wild type and AMPKα2 knockout (AMPKα2(-/-)) littermates were subjected to left ventricular pressure overload caused by transverse aortic constriction. After administration of metformin (200 mg·kg(-1)·d(-1)) for 6 weeks, the degree of cardiac hypertrophy was evaluated using echocardiography and anatomic and histological methods. The antihypertrophic mechanism of metformin was analyzed using Western blotting.Results:Metformin significantly attenuated cardiac hypertrophy induced by pressure overload in wild type mice, but the antihypertrophic actions of metformin were ablated in AMPKα2(-/-) mice. Furthermore, metformin suppressed the phosphorylation of Akt/protein kinase B (AKT) and mammalian target of rapamycin (mTOR) in response to pressure overload in wild type mice, but not in AMPKα2(-/-) mice.Conclusion:Long-term administration of metformin may attenuate cardiac hypertrophy induced by pressure overload in nondiabetic mice, and this attenuation is highly dependent on AMPK activation. These findings may provide a potential therapy for patients at risk of developing pathological cardiac hypertrophy. |
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Authors:
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Yong-Nan Fu; Han Xiao; Xiao-Wei Ma; Sheng-Yang Jiang; Ming Xu; You-Yi Zhang |
Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-5-09 |
Journal Detail:
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Title: Acta pharmacologica Sinica Volume: - ISSN: 1745-7254 ISO Abbreviation: - Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-5-9 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100956087 Medline TA: Acta Pharmacol Sin Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100191, China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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