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• W9393729 abstract "Cardiovascular diseases (CVDs) and their treatment pose a huge economic and social burden in Western societies and in the developing world (1). Thus, there is significant interest in developing new therapeutic targets, and it is of particular interest that an old class of drugs, inhibitors of xanthine oxidoreductase (XO), may be repositioned to treat heart failure and left ventricular (LV) dysfunction. In this context, there is growing awareness that nitroso-redox balance may represent a new therapeutic target for heart failure (2). However, whether or not XO inhibitors fully address nitroso-redox imbalance in all patients remains controversial.The hypothesis that XO inhibition could treat heart failure was tested in the OPT-CHF trial (3). In that study, the primary endpoint was not statistically different in the population of symptomatic heart failure patients enrolled; however patients with hyperuricemia appeared to be a responsive population. While hyperuricemia is classically associated with gout and nephropathy, it is clearly also a biomarker in heart failure populations (4-6). Uric acid (UA) is the end product of purine metabolism, involving the conversion of hypoxanthine to xanthine and then to UA in reactions catalyzed by XO (Figure 1) (7). In most mammals including rodents, UA is further degraded to allantoin via the enzyme urate oxidase (UO), resulting in low UA serum levels. In humans and great apes, however, this final step does not occur because of a single point mutation inactivating UO, resulting in substantially higher serum UA levels. Whether UA plays beneficial or deleterious roles remains controversial, and some arguments can be made that the impact of UA on vascular tone have played an evolutionary role (4). However, in hypertension, type 2 diabetes mellitus, coronary artery disease (CAD), heart failure, and chronic kidney disease (CKD), high UA levels correlate with an increased risk of stroke and CVDs (4,6,8-10)Figure 1Increased xanthine oxidase activity and nitroso-redox imbalanceAs UA levels represent a biomarker of XO activity, the OPT-CHF results suggest that patients with elevated XO activity responded preferentially (3). XO is a key oxidase participating in nitroso-redox imbalance in the heart, producing superoxide as a byproduct of purine metabolism (Figure 1). Thus, the epidemiological association of high UA levels with worse prognosis in a wide cohort of patients with CVDs likely reflects the fact that UA levels rise with increased XO activity (4-10)." @default.
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• W9393729 date "2013-03-01" @default.
• W9393729 modified "2023-10-12" @default.
• W9393729 title "Nitroso-Redox Imbalance Affects Cardiac Structure and Function" @default.
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• W9393729 doi "https://doi.org/10.1016/j.jacc.2012.12.016" @default.
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