![]() |
JOURNAL TOOLS |
eTOC |
Per abbonarsi |
Sottometti un articolo |
Segnala alla tua biblioteca |
ARTICLE TOOLS |
Estratti |
Permessi |

I TUOI DATI
I TUOI ORDINI
CESTINO ACQUISTI
N. prodotti: 0
Totale ordine: € 0,00
COME ORDINARE
I TUOI ABBONAMENTI
I TUOI ARTICOLI
I TUOI EBOOK
COUPON
ACCESSIBILITÀ
REVIEWS
Panminerva Medica 2005 September;47(3):169-86
Copyright © 2009 EDIZIONI MINERVA MEDICA
lingua: Inglese
Role of transforming growth factor-beta 1/Smads in regulating vascular inflammation and atherogenesis
Feinberg M. W., Jain M. K.
The Program in Cardiovascular Transcriptional Biology Cardiovascular Division Brigham and Women’s Hospital Harvard Medical School, Boston, MA, USA
Accumulating evidence supports the role of inflammation in the development of a variety of chronic vascular diseases such as atherosclerosis, transplantation arteriosclerosis, and restenosis after vascular mechanical injury. Thus, identification of mechanisms to control inflammation may provide novel therapeutic targets to limit such disease states. Transforming growth factor-beta1 (TGF-β1) is a pleiotropic growth factor with potent immunomodulating effects on cells important to atherosclerotic lesion formation including endothelial cells, vascular smooth muscle cells, macrophages, and T cells. The mechanisms responsible for the protective, anti-inflammatory effects of TGF-β1 have recently become elucidated. This review focuses on the emerging role of the downstream TGF-β1 signaling mediators, termed Smads, as regulators of vascular inflammation. These findings are beginning to establish a mechanistic scaffold with which to understand the cell-type specific function of Smads in the development of chronic inflammatory vascular disease states.