Linked Life Data

8835864

Source:http://linkedlifedata.com/resource/pubmed/id/8835864

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-2-24
pubmed:abstractText
In recent years, the striking development of molecular biology and molecular genetic has brought completely new insights into the understanding of heart failure. Two aspects for which significant progress has been made in 1995 are discussed in this review: the genetic mechanisms of inherited cardiomyopathies and the molecular basis of heart failure due to chronic hemodynamic overload. In familial hypertrophic cardiomyopathy, a novel disease gene was found. It encodes myosin binding protein C, whose structure and function are poorly understood. Contractile deficits associated with the myosin mutations were demonstrated, and all this strengthened the hypothesis that hypertrophy is a compensatory mechanism that occurs in presence of a sarcomeric defect. These studies have important prognostic and clinical implications, but new and unexpected concerns have arisen, because a widespread difference in phenotype can be seen in patients harboring similar genotypes. In familial dilated cardiomyopathy, the main findings were the identification of four disease loci, but the genes are still unknown. With respect to the consequences of chronic hemodynamic overload on myocyte function and phenotype, recent data gave rise to lively discussions in the fields of reexpression of fetal troponin T isoforms and of decreased function and expression of the sarco(endo)plasmic reticulum Ca2+ ATPase in the failing human heart; at the moment it is difficult to draw definitive conclusions. Interestingly, three new concepts emerged in the understanding of the pathogenesis of heart failure: the increased contribution of the Na(+)-Ca2+ exchange, the possible recruitment of an inositol phosphate-sensitive calcium pool for myofibrillar activation, and the involvement of apoptotic myocyte and nonmyocyte cell death in myocardial remodeling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0268-4705
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
227-36
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Molecular and cellular biology of heart failure.
pubmed:affiliation
INSERM Unité 153, Groupe Hospitalier Pitié-Salpêtrière, Paris, France.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't