Abstract
Serum uric acid (SUA) is considered a marker and possible factor of nature progression of chronic heart failure (CHF) mediated cardiovascular remodelling. Recent investigations have shown that SUA is independent and strong predictor of outcome in the general population as well as in patients with cardiovascular and non-cardiovascular diseases, such as myocardial infarction, acute coronary syndrome, acute and chronic cardiac failure, type 2 diabetes mellitus, atherosclerosis, the metabolic syndrome, chronic kidney disease, and obstructive sleep apnea syndrome. It has suggested that SUA may contribute in controversial mechanisms that relate with prooxidative and antioxidative state. Because uric acid is able to activate intracellular signaling system affected Akt / STAT / MAP-kinase mechanisms, there is predisposition that SUA may mediate with mobbing and differentiation of mononuclear progenitor cells (MPCs). The review is addressed to discussion of one of possible mechanism of effect realizing of SUA in heart failure affected endogenous reparation via endothelial proangiogenic MPCs.
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