Oxidative stress via H2O2 activates key signaling pathways (MAPKs and PKB/Akt) in vascular smooth muscle cells, providing a molecular mechanism for its role in vascular diseases like atherosclerosis and hypertension.
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.
Blanc et al. (2003) studied this question.