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Metformin attenuates pressure overload-induced cardiac hypertrophy via AMPK activation.
MedLine Citation:
PMID:  21552292     Owner:  NLM     Status:  Publisher    
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.
Yong-Nan Fu; Han Xiao; Xiao-Wei Ma; Sheng-Yang Jiang; Ming Xu; You-Yi Zhang
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-5-09
Journal Detail:
Title:  Acta pharmacologica Sinica     Volume:  -     ISSN:  1745-7254     ISO Abbreviation:  -     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-5-9     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100956087     Medline TA:  Acta Pharmacol Sin     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
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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