Corresponding author:Alexander E. Berezin, Professor, MD, PhD, Private Clinic “Vita-Center”, 3, Sedova str, Senior Consultant of Therapeutic Unit, Internal Medicine Department, State Medical University of Zaporozhye, 26, Mayakovsky av, Zaporozhye, Ukraine
Received: July 31, 2017; Published: August 03, 2017
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The majority of individuals with traditional cardiovascular risk factors contributing in heart failure (HF) risk exhibited increased serum levels of uric acid. The role of SUA in HF manifestation appears to be controversial. First controversy affects the fact that SUA plays an important role in inducing oxidative stress, inflammation, neuro humoral activation, and endothelial dysfunction. Being natural antioxidant uric acid contributes in prevention of cell damage and thereby may restore vascular function leading to reversion of endothelial dysfunction. Interestingly, there is a large body of evidence regarding that uric acid is able to regulate an activity of endogenous repair system through epigenetic mechanisms and activation of intracellular signaling, such as STAT3 and Akt. Indeed, uric acid mediates a survival of endothelial precursors, mediate their mobbing and differentiation, as well as coordinate a turn-over effect of metabolic memory phenomenon into repair capability of cell precursors. Probably, these controversies could have taken into consideration when clinical results of several studies are discussed. Although elevated SUA levels were found a strong predictor of adverse clinical outcomes in HF patients, there is assumption that final result of elevated uric acid may depend on cooperation between metabolic and epigenetic factors contributing in HF evolution. The short communication is depicted the importance of new clinical data to confirm the emerging reparative ability of SUA in HF and its role as promising target for treatment in cardiac failure.