Van Eyk, Dunn - Proteomic and Genomic Analysis of Cardiovascular Disease - 2003 (522919), страница 84
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Within the vessel wall, ROS are generated byseveral mechanisms, including a vascular NAD(P)H oxidase [5, 6]. ROS formationcan be stimulated by mechanical stress, environmental factors, platelet-derivedgrowth factor (PDGF), angiotensin II (Ang II), and low-density lipoproteins [7-9].Because many risk factors for coronary artery disease such as hyperlipidemia, hypertension, diabetes, and smoking increase production of ROS, it has been suggested that changes in vessel redox state are a common pathway involved in thepathogenesis of atherosclerosis [1, 6, 10]. We have previously reported that ROSstimulate vascular smooth muscle cell (VSMC) growth and DNA synthesis [11].This proliferation was associated with stimulation of protein kinases, especiallythe extracellular signal-regulated kinases (ERK1/2) [4].Activation of ERK1/2 by O–2 generators such as the napthoquinolinedioneLY83583, menadione, and xanthine/xanthine oxidase was biphasic: an early peakof ERK1/2 activity was present at 5 to 10 min, whereas a delayed ERK1/2 activation appeared at 2 hour [12].