Document Detail

Physiological myocardial hypertrophy: how and why?
MedLine Citation:
PMID:  17981549     Owner:  NLM     Status:  MEDLINE    
Cardiac hypertrophy is defined by augmentation of ventricular mass as a result of increased cardiomyocyte size, and is the adaptive response of the heart to enhanced hemodynamic loads due to either physiological stimuli (post-natal developmental growth, training, and pregnancy) or pathological states (such as hypertension, valvular insufficiency, etc). The mechanisms leading to hypertrophy during pathological and physiological states are distinct but, in general, evidence indicates that hypertrophy results from the interaction of mechanical forces and neurohormonal factors. Hemodynamic overload creates a mechanical burden on the heart and results in stretch of the myocyte and induction of gene expression of cardiac growth factors. Insulin-like growth factor 1 (IGF1) has recently been shown to be the most important cardiac growth factor involved in physiological hypertrophy. In this review, IGF1 and the pathways it triggers will be discussed.
Daniele Catalucci; Michael V G Latronico; Oyvind Ellingsen; Gianluigi Condorelli
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2008-01-01
Journal Detail:
Title:  Frontiers in bioscience : a journal and virtual library     Volume:  13     ISSN:  1093-4715     ISO Abbreviation:  Front. Biosci.     Publication Date:  2008  
Date Detail:
Created Date:  2007-11-05     Completed Date:  2007-12-11     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  9709506     Medline TA:  Front Biosci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  312-24     Citation Subset:  IM    
Department of Medicine, Division of Cardiology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0613, USA.
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MeSH Terms
1-Phosphatidylinositol 3-Kinase / metabolism
Cell Proliferation
Insulin-Like Growth Factor I / metabolism
Models, Biological
Myocardium / pathology*
Neovascularization, Pathologic
Proto-Oncogene Proteins c-akt / metabolism
Receptors, Adrenergic / metabolism
Signal Transduction
Grant Support
Reg. No./Substance:
0/Receptors, Adrenergic; 67763-96-6/Insulin-Like Growth Factor I; EC 3-Kinase; EC Proteins c-akt

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