Uric Acid in Heart Failure: Controversy Factor in The Multiple Pathogenesis of The Disease
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2017, Vol 1, Issue 3
Abstract
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.TThere is a large body of evidence regarding the role of serum uric acid (SUA) in pathogenesis of cardiovascular diseases (CVD) including heart failure (HF). Recent clinical studies and some meta-analysis have shown that elevated SUA was associated with an increased risk of incident HF, observed in majority of patients with established chronic HF and relate to adverse clinical outcomes in HF [1-4]. However, the impact of SUA on all-cause mortality and HF-related death was insured by co-existing disease predominantly hypertension, abdominal obesity, pred iabetes / diabetes mellitus, kidney disease as well as female sex [2,5-7]. Whether SUA could be an independent predictor of HF development is not fully clear. Moreover, there are data clarifying that even asymptomatic hyperuricemia associated strongly with long-term survival of CVD patients and individuals with chronic kidney disease throughout pre-dialysis period and whose who undergoing hemodialysis procedures.
Authors and Affiliations
Alexander E Berezin
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