Linked Life Data

12711218

Source:http://linkedlifedata.com/resource/pubmed/id/12711218

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-4-24
pubmed:abstractText
Genetic analysis of hypertrophic cardiomyopathy (HCM), a mendelian form of cardiac hypertrophy, indicates that the primary defect is in sarcomeric function. However, the initial proposal that depressed myocardial contraction leads to a 'compensatory' hypertrophy has proven inconsistent with laboratory and clinical evidence. Drawing on observations of mutant contractile protein function, together with mouse models and clinical studies, we propose that sarcomeric HCM mutations lead to inefficient ATP utilization. The suggestion that energy depletion underlies HCM is supported by the HCM-like phenotype found with mutations in a variety of metabolic genes. A central role for compromised energetics would also help explain the unresolved clinical observations of delayed onset and asymmetrical hypertrophy in HCM, and would have implications for therapy in HCM and, potentially, in more-common forms of cardiac hypertrophy and failure.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0168-9525
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
263-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Hypertrophic cardiomyopathy:a paradigm for myocardial energy depletion.
pubmed:affiliation
Department of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't