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Conference Paper: Switches in cardiac muscle gene expression as a result of pressure and volume overload

TitleSwitches in cardiac muscle gene expression as a result of pressure and volume overload
Authors
Issue Date1992
Citation
American Journal of Physiology - Regulatory Integrative and Comparative Physiology, 1992, v. 262 n. 3 31-3, p. R364-R369 How to Cite?
AbstractIn the mammalian heart, the expression of genes encoding proteins responsible for contraction, relaxation, and endocrine function changes in hypertrophy resulting from hemodynamic overload. Different mechanisms are involved in this mechanogenic transduction, including 1) differential expression of myosin and actin multigene families, which may account for the decreased velocity of contractile element shortening in hypertrophied heart, 2) nonactivation of the sarcoplasmic reticulum Ca2+-ATPase gene, which may explain the increased duration of isometric relaxation, and finally 3) activation in the ventricle of the atrial natriuretic factor gene that is responsible in part for the high plasma levels of this peptide. It is increasingly apparent that these changes are independently regulated, but little is known about the mechanisms underlying this regulation. Preliminary results indicate that it is now possible to analyze the early time course or transcription for each gene after the imposition of hemodynamic overload. This should significantly enhance our understanding of the regulatory mechanisms involved in the phenoconversions of the hemodynamically overloaded heart.
Persistent Identifierhttp://hdl.handle.net/10722/195225
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorSchwartz, K-
dc.contributor.authorBoheler, KR-
dc.contributor.authorDe la Bastie, D-
dc.contributor.authorLompre, A-M-
dc.contributor.authorMercadier, J-J-
dc.date.accessioned2014-02-25T01:40:19Z-
dc.date.available2014-02-25T01:40:19Z-
dc.date.issued1992-
dc.identifier.citationAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology, 1992, v. 262 n. 3 31-3, p. R364-R369-
dc.identifier.issn0002-9513-
dc.identifier.urihttp://hdl.handle.net/10722/195225-
dc.description.abstractIn the mammalian heart, the expression of genes encoding proteins responsible for contraction, relaxation, and endocrine function changes in hypertrophy resulting from hemodynamic overload. Different mechanisms are involved in this mechanogenic transduction, including 1) differential expression of myosin and actin multigene families, which may account for the decreased velocity of contractile element shortening in hypertrophied heart, 2) nonactivation of the sarcoplasmic reticulum Ca2+-ATPase gene, which may explain the increased duration of isometric relaxation, and finally 3) activation in the ventricle of the atrial natriuretic factor gene that is responsible in part for the high plasma levels of this peptide. It is increasingly apparent that these changes are independently regulated, but little is known about the mechanisms underlying this regulation. Preliminary results indicate that it is now possible to analyze the early time course or transcription for each gene after the imposition of hemodynamic overload. This should significantly enhance our understanding of the regulatory mechanisms involved in the phenoconversions of the hemodynamically overloaded heart.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology-
dc.titleSwitches in cardiac muscle gene expression as a result of pressure and volume overload-
dc.typeConference_Paper-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid1532697-
dc.identifier.scopuseid_2-s2.0-0026605560-
dc.identifier.volume262-
dc.identifier.issue3 31-3-
dc.identifier.spageR364-
dc.identifier.epageR369-
dc.identifier.isiWOS:A1992HK36400053-

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