Document Detail


Physiological myocardial hypertrophy: how and why?
MedLine Citation:
PMID:  17981549     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Daniele Catalucci; Michael V G Latronico; Oyvind Ellingsen; Gianluigi Condorelli
Related Documents :
2589159 - Anatomic findings in acute papillary muscle necrosis.
2137959 - Survival determinants in black patients with angiographically defined coronary artery d...
8395169 - Local expression and pathophysiological role of renin-angiotensin in the blood vessels ...
1827699 - Echocardiographic and pulsed doppler features in glycogen storage disease type ii of th...
8166049 - Molecular basis of regression of cardiac hypertrophy.
3402469 - Acute right ventricular infarction secondary to massive pulmonary embolism.
23105879 - Circulating thrombotic and haemostatic components in patients with coronary artery dise...
2968479 - Myocardial interstitial fibrosis in experimental uremia--implications for cardiac compl...
11323779 - Renal infarct: contrast-enhanced power doppler sonographic findings.
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    
Affiliation:
Department of Medicine, Division of Cardiology, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0613, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
1-Phosphatidylinositol 3-Kinase / metabolism
Animals
Cell Proliferation
Female
Humans
Hypertrophy
Insulin-Like Growth Factor I / metabolism
Male
Models, Biological
Myocardium / pathology*
Neovascularization, Pathologic
Pregnancy
Proto-Oncogene Proteins c-akt / metabolism
Receptors, Adrenergic / metabolism
Signal Transduction
Grant Support
ID/Acronym/Agency:
R0 HL078797-01A1/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Adrenergic; 67763-96-6/Insulin-Like Growth Factor I; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt

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


Previous Document:  Impact of physical exercise on alterations in the skeletal muscle in patients with chronic heart fai...
Next Document:  Heart failure and cachexia: insights offered from molecular biology.