Document Detail

Novel insights into the role of cardiotrophin-1 in cardiovascular diseases.
MedLine Citation:
PMID:  19059413     Owner:  NLM     Status:  MEDLINE    
Cardiotrophin-1 (CT-1), a member of interleukin (IL)-6 family, was originally isolated for its ability to induce a hypertrophic response in neonatal cardiac myocytes. This cytokine mediates a pleiotropic set of growth and differentiation activities through a unique receptor system, consisting of IL-6 receptor (IL-6R) and a common signal transducer, the glycoprotein 130 (gp130). Both in humans and in mice, CT-1 mRNA has been detected in several tissues, such as liver tissue, adipose tissue, and tissues in the respiratory and nervous systems; in each of these tissues it performs different functions. Predominant actions of CT-1 are on the heart, where it is synthesized and where it provides first myocardial protection by promoting cell survival and proliferation, it carries on its haemodynamic effects and endocrine properties, and finally, it predisposes the heart to pathological conditions. The aim of this review is to describe the pathophysiological mechanisms through which CT-1 carries out its activities, especially on the heart, and its potential contribution as a disease marker in clinical cardiology. Recent studies have confirmed its active role in promoting structural changes typical of most common cardiovascular disease, such as hypertension, valve diseases, congestive heart failure, and coronary artery disease. In fact, CT-1 induces myocyte hypertrophy and collagen synthesis, thereby participating in the progression of ventricular remodelling, which results in cardiac muscle failure at the latest stage. CT-1 plasma levels are elevated in patients with hypertension and coronary artery diseases, and they are also correlated with the severity of valve diseases and heart failure. Therefore, CT-1 may represent a diagnostic, staging, and prognostic biomarker of cardiovascular diseases.
P Calabrò; G Limongelli; L Riegler; V Maddaloni; R Palmieri; E Golia; T Roselli; D Masarone; G Pacileo; P Golino; R Calabrò
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Publication Detail:
Type:  Journal Article; Review     Date:  2008-11-13
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  46     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2009 Feb 
Date Detail:
Created Date:  2009-01-16     Completed Date:  2009-05-05     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  142-8     Citation Subset:  IM    
Division of Cardiology, Second University of Naples-A.O. Monaldi, Via L. Bianchi, 80131 Naples, Italy.
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MeSH Terms
Cardiovascular Diseases / genetics,  metabolism*,  pathology
Cytokines / genetics,  metabolism*,  physiology*
Models, Biological
Myocytes, Cardiac / metabolism,  pathology
Signal Transduction / genetics,  physiology
Reg. No./Substance:
0/Cytokines; 0/cardiotrophin 1

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