Copyright © 2007, European Society of Cardiology
The TGFβ superfamily in cardiovascular biology
aDepartment of Internal Medicine and Physiology and Biophysics, University of Arkansas for Medical Sciences and Central Arkansas Veterans Healthcare System, Little Rock, Arkansas, USA
bInstitute for Surgical Research, Rikshospitalet University Hospital, Oslo, Norway
* Corresponding author. Division of Cardiovascular Medicine, University of Arkansas for Medical Sciences, 4301 West Markham St., Slot 532, Little Rock, 72205-7199 AR, USA. Tel.: +1 501 296 1401; fax: +1 501 686 8319. Email address: MehtaJL@uams.edu
Received 9 March 2007; accepted 12 March 2007
| The first 10% of the full text of this article appears below. |
| 1. The biology of the TGFβ superfamily |
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This issue of Cardiovascular Research is focused on the TGFβ superfamily and cardiovascular disease. It is timely to comment on some of the unique aspects of this potent cytokine family in relation to cardiovascular disease. There are three structurally similar isoforms of TGFβ, encoded by three distinct genes, in mammalian species; of these, TGFβ1 is the most prevalent. The TGFβ superfamily also includes several other related growth factors, including activin, GDF-15, several bone morphogenetic protein (BMP) isoforms, and nodal. Apparently, all TGFβ superfamily members bind to heterodimeric receptor isomers that belong to the same family, i.e. dimeric complexes of various type I receptor serine/threonine kinases (ALK 1-7) and type II receptor proteins (5 isoforms). These receptors subsequently activate different intracellular Smad proteins
| 2. TGFβ and atherosclerosis |
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| 3. Myocardial ischemia and cardiac remodeling |
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