Linked Life Data

14745128

Source:http://linkedlifedata.com/resource/pubmed/id/14745128

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-1-27
pubmed:abstractText
Cytosolic Ca(2+) is a key regulator of excitation-contraction coupling in myocardium. Myocardial contractile dysfunction in heart failure is characterized by a decrease in contraction and prolonged relaxation. These alterations are mainly due to changes in 1) intracellular Ca(2+) transients (CaT), 2) Ca(2+) sensitivity of the contractile elements, and/or 3) contractile proteins. It is useful to investigate the relationship between CaT and contraction for understanding of the mechanism of contractile dysfunction in heart failure. There are many reports regarding the alterations in CaT, Ca(2+) sensitivity, and contractile proteins in heart failure. Changes in the activity of the sarcoplasmic Ca(2+) pump protein, SERCA2a, may be involved in the altered contractility in heart failure. We generated cardiac-restricted overexpression of SERCA2a transgenic mice (TG) and non-transgenic littermates (NTG). To investigate the role of SERCA2a activity for ischemic heart, we used acidosis as a model of acute contractile dysfunction. During acidosis and recovery from acidosis, the peaks of CaT and tension in TG were significantly larger than those in NTG. These results suggest that an increase in the activity of SERCA2a could be beneficial to preserve contractility during acidosis and recovery. Thus, a disturbance of the intracellular Ca(2+) homeostasis is one of the key factors for the contractile dysfunction in heart failure.
pubmed:language
jpn
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0015-5691
pubmed:author
pubmed:issnType
Print
pubmed:volume
123
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
87-93
pubmed:dateRevised
2011-7-27
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
[The mechanism of contractile dysfunction in heart failure, focussing on SERCA2a function].
pubmed:affiliation
Department of Physiology (II), The Jikei University School of Medicine, Tokyo, Japan. kusakari@jikei.ac.jp
pubmed:publicationType
Journal Article, English Abstract, Review