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Cited by 406

The DOI matches its Crossref record; 123 of the 123 references it cites were found in a registry or an index.

Uric acid, hyperuricemia and vascular diseases

Open access
Jin, Ming·2012·Frontiers in Bioscience
DOI 10.2741/3950
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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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Metadata

Authors
Jin, M.
Venue
Frontiers in Bioscience
Publisher
IMR Press
Published
2012
Volume
17
Issue
1
Pages
656
ISSN
  • 1093-4715 (ISSN-L)
  • 1093-9946
DOI
10.2741/3950
OpenAlex
W2045185413
Cited by
406
References
123
FWCI
8.33
Type
journal article
Language
en
Open access
bronze

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

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