Linked Life Data

16039971

Source:http://linkedlifedata.com/resource/pubmed/id/16039971

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2005-7-25
pubmed:abstractText
AMP-activated protein kinase (AMPK) is activated during exercise and ischemia and is emerging as an important regulatory mechanism in the heart. AMPK promotes adenosine triphosphate-generating pathways, including glucose transport, glycolysis, and fatty acid oxidation, while inhibiting energy-consuming anabolic pathways. After ischemia-reperfusion, AMPK-deficient hearts from transgenic mice have severe left ventricular contractile dysfunction with increased apoptosis and necrosis. Mutations in the AMPKgamma(2) subunit lead to cardiac glycogen overload, Wolff-Parkinson-White syndrome, arrhythmias, and heart failure. This review focuses on the molecular mechanisms of activation and cardiovascular actions of AMPK in the heart.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1050-1738
pubmed:author
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
110-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
AMP-activated protein kinase: a key stress signaling pathway in the heart.
pubmed:affiliation
Department of Internal Medicine, Section of Cardiovascular Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. lawrence.young@yale.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, N.I.H., Extramural