Open Access
Review
Uric acid, hyperuricemia and vascular diseases
Ming Jin1,4,Fan Yang4,Irene Yang4,Ying Yin2,4,Jin Jun Luo3,4,Hong Wang2,4,Xiao-Feng Yang2,4,*
1
Department of Pathology and Laboratory Medicine, Philadelphia, PA 19140
2
Department of Pharmacology and Cardiovascular Research Center, Philadelphia, PA 19140
3
Department of Neurology, Philadelphia, PA 19140
4
Temple University School of Medicine, Philadelphia, PA 19140
DOI: 10.2741/3950 Volume 17 Issue 2, pp.656-669
Published: 01 January 2012
*Corresponding Author(s):  
Xiao-Feng Yang
E-mail:  
xfyang@temple.edu
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.

Key words

Uric acid, Hyperuricemia, Cardiovascular disease, Inflammasome, Review

Share and Cite
Ming Jin, Fan Yang, Irene Yang, Ying Yin, Jin Jun Luo, Hong Wang, Xiao-Feng Yang. Uric acid, hyperuricemia and vascular diseases. Frontiers in Bioscience-Landmark. 2012. 17(2); 656-669.