Document Detail

Novel regulators and drug targets of cardiac hypertrophy.
MedLine Citation:
PMID:  20823714     Owner:  NLM     Status:  MEDLINE    
Cardiac hypertrophy is classically considered as an adaptive and compensatory response enabling cardiomyocytes to increase their work output and thus cardiac function. Biomechanical stress and neurohumoral activation are the most important triggers of pathological hypertrophy and the transition of cardiac hypertrophy to heart failure. Several novel regulators and putative drug targets of cardiac hypertrophy have been found by using gene-modified and acquired models of cardiac hypertrophy. Recent studies have also revealed distinct patterns of cardiac substrate utilization in cardiac hypertrophy and heart failure. The use of novel systems biology techniques such as metabolomics may therefore in future provide insights into the metabolic processes and cardiovascular biology related to cardiac hypertrophy and also extend the ability to discover circulating biomarkers for cardiovascular diseases. The present review discusses current knowledge on molecular mechanisms of cardiac hypertrophy, with special emphasis on novel regulators and putative drug targets of cardiac hypertrophy such as the tissue renin-angiotensin-aldosterone system, calcineurin/nuclear factor of activated T cells pathway, phosphatidylinositol 3-kinase/growth promoting protein kinase B, mammalian target of rapamycin, histone deacetylases, AMPkinases, microRNAs and angiogenetic factors.
Piet Finckenberg; Eero Mervaala
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Journal of hypertension     Volume:  28 Suppl 1     ISSN:  1473-5598     ISO Abbreviation:  J. Hypertens.     Publication Date:  2010 Sep 
Date Detail:
Created Date:  2010-09-08     Completed Date:  2011-01-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  S33-8     Citation Subset:  IM    
Institute of Biomedicine, University of Helsinki, Finland.
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MeSH Terms
AMP-Activated Protein Kinases / metabolism
Angiogenesis Inducing Agents / metabolism
Calcineurin / metabolism
Cardiomegaly / drug therapy*,  metabolism
Histone Deacetylases / metabolism
MicroRNAs / metabolism
Renin-Angiotensin System / drug effects*
TOR Serine-Threonine Kinases / metabolism
Reg. No./Substance:
0/Angiogenesis Inducing Agents; 0/MicroRNAs; EC Serine-Threonine Kinases; EC Protein Kinases; EC; EC Deacetylases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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