Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate
AbstractThe generation of reactive oxygen species (ROS) and an imbalance of antioxidant defence mechanisms can result in oxidative stress. Several pro-atherogenic stimuli that promote intimal-medial thickening (IMT) and early arteriosclerotic disease progression share oxidative stress as a common regulatory pathway dictating vascular cell fate. The major source of ROS generated within the vascular system is the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes (Nox), of which seven members have been characterized. The Nox family are critical determinants of the redox state within the vessel wall that dictate, in part the pathophysiology of several vascular phenotypes. This review highlights the putative role of ROS in controlling vascular fate by promoting endothelial dysfunction, altering vascular smooth muscle phenotype and dictating resident vascular stem cell fate, all of which contribute to intimal medial thickening and vascular disease progression. View Full-Text
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Burtenshaw, D.; Hakimjavadi, R.; Redmond, E.M.; Cahill, P.A. Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate. Antioxidants 2017, 6, 90.
Burtenshaw D, Hakimjavadi R, Redmond EM, Cahill PA. Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate. Antioxidants. 2017; 6(4):90.Chicago/Turabian Style
Burtenshaw, Denise; Hakimjavadi, Roya; Redmond, Eileen M.; Cahill, Paul A. 2017. "Nox, Reactive Oxygen Species and Regulation of Vascular Cell Fate." Antioxidants 6, no. 4: 90.
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