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Mechanistic hypothesis based on the published data and the results of the present study. A vicious cycle is created in which renal cysts activate the RAAS, and the resulting increase in Ang II leads to oxidative stress, vascular inflammation, and endothelial dysfunction. AngII, angiotensin II; HODE, hydroxy-octadecadienoic acid; LOX, lipoxygenases; RAAS, renin-angiotensin-aldosterone system.
