Mechanical integrity of arteries is vital for maintaining compensatory mechanisms under physiologic conditions, and changes in vessel structure (and consequently, vessel mechanical properties) are hallmarks of the progression of pathologic states. Oxidative stress can (1) induce endothelial dysfunction by interfering with nitric oxide (NO) signaling pathways relevant to vasodilation/vasoconstriction of arteries, and (2) alter atherosclerotic plaque composition by oxidation of constituents or by interruption of reverse cholesterol transport from plaques.

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