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ROS in Atherosclerotic Renovascular Disease

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Studies on Atherosclerosis

Abstract

The hallmark of atherosclerotic renovascular disease (ARVD) is activation of the renin-angiotensin-aldosterone system, in which Ang II induces NAD(P)H oxidase-derived reactive oxygen species (ROS). Renovascular hypertension may also induce oscillatory shear stress, which is linked to increased ROS production with consequent oxidative damage. Induction of these signaling cascades leads to expression of pro-inflammatory mediators, cell apoptosis, and modification of extracellular matrix, eventuating in endothelial dysfunction, glomerulosclerosis, microvascular rarefaction, and tissue fibrosis. ROS-mediated kidney injury, primarily in the stenotic and also in the contralateral kidney, impair renal function. Intervention with antioxidants has the potential to improve renal function in experimental setting but failed to translate into clinical outcome. Angiotensin converting enzyme inhibitor/angiotensin receptor blockers have showed potential of attenuation of oxidative stress while improving clinical outcome. Stem cells combined with percutaneous transluminal renal angioplasty has promising results in experimental ARVD and translational studies are urgently needed in this area.

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Correspondence to Lilach O. Lerman M.D., Ph.D. .

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Zhu, XY., Lerman, L.O. (2017). ROS in Atherosclerotic Renovascular Disease. In: Rodriguez-Porcel, M., Chade, A., Miller, J. (eds) Studies on Atherosclerosis. Oxidative Stress in Applied Basic Research and Clinical Practice. Humana Press, Boston, MA. https://doi.org/10.1007/978-1-4899-7693-2_2

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