Synchronous activation of ERK 1/2, p38mapk and PKB/Akt signaling by H2O2 in vascular smooth muscle cells: potential involvement in vascular disease (review).
Int J Mol Med
; 11(2): 229-34, 2003 Feb.
Article
em En
| MEDLINE
| ID: mdl-12525883
ABSTRACT
Oxidative stress has been implicated in the pathogenesis of a host of vascular abnormalities such as atherosclerosis, hypertension and in restenosis followed by balloon angioplasty. However, the molecular mechanism by which oxidative stress causes these abnormalities remains poorly characterized. Recent studies have shown that exposure of vascular smooth muscle cells (VSMC) with H2O2, to mimic oxidative stress, activates components of growth promoting and proliferative signal transduction pathways. These components include mitogen-activated protein kinases (MAPKs) and protein kinase B (PKB/Akt), and are believed to be key players mediating growth, proliferation, hypertrophy, migration, survival and death of VSMC. We provide a brief overview of the effect of H2O2 on MAPKs and PKB/Akt signaling in VSMC in relation to their potential role in the pathogenesis of vascular diseases.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Doenças Vasculares
/
Transdução de Sinais
/
Proteínas Serina-Treonina Quinases
/
Peróxido de Hidrogênio
/
Músculo Liso Vascular
Limite:
Animals
/
Humans
Idioma:
En
Ano de publicação:
2003
Tipo de documento:
Article