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Review
. 2012 Jan 1;17(2):656-69.
doi: 10.2741/3950.

Uric acid, hyperuricemia and vascular diseases

Ming Jin  1 , Fan Yang, Irene Yang, Ying Yin, Jin Jun Luo, Hong Wang, Xiao-Feng Yang
Affiliations
Review

Uric acid, hyperuricemia and vascular diseases

Ming Jin et al. Front Biosci (Landmark Ed). .

Abstract

Uric acid is the product of purine metabolism. It is known that hyperuricemia, defined as high levels of blood uric acid, is the major etiological factor of gout. A number of epidemiological reports have increasingly linked hyperuricemia with cardiovascular and neurological diseases. Studies highlighting the pathogenic mechanisms of uric acid point to an inflammatory response as the primary mechanism for inducing gout and possibly contributing to uric acid's vascular effects. Monosodium urate (MSU) crystals induce an inflammatory reaction, which are recognized by toll-like receptors (TLRs). These TLRs then activate NALP3 inflammasome. MSU also triggers neutrophil activation and further produces immune mediators, which lead to a proinflammatory response. In addition, soluble uric acid can also mediate the generation of free radicals and function as a pro-oxidant. This review summarizes the epidemiological studies of hyperuricemia and cardiovascular disease, takes a brief look at hyperuricemia and its role in neurological diseases, and highlights the studies of the advanced pathological mechanisms of uric acid and inflammation.

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Figures

Fig. 1
Fig. 1. Biosynthesis of uric acid
Abbreviations: AMP: adenosine monophosphate; IMP: inosine monophosphate; XMP: xanthosine monophosphate; GMP: guanosine monophosphate; NT: nucleotidase; PNP: purine nucleoside phosphorylase; HGPRT: hypoxanthine-guanine phosphoribosyltransferase
Fig. 2
Fig. 2
Mechanisms and pathways in MSU-mediated inflammation
Fig. 3
Fig. 3
Hyperuricemia and diseases
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