期刊
FRONTIERS IN BIOSCIENCE-LANDMARK
卷 17, 期 -, 页码 656-669出版社
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/3950
关键词
Uric acid; Hyperuricemia; Cardiovascular disease; Inflammasome; Review
资金
- NHLBI NIH HHS [R01 HL077288, R01 HL094451-02, R01 HL117654, R01 HL094451] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL094451, R01HL117654, R01HL077288] Funding Source: NIH RePORTER
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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