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Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis

Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive...

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Detalles Bibliográficos
Autores principales: Kimura, Yoshitaka, Tsukui, Daisuke, Kono, Hajime
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8624633/
https://www.ncbi.nlm.nih.gov/pubmed/34830282
http://dx.doi.org/10.3390/ijms222212394
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author Kimura, Yoshitaka
Tsukui, Daisuke
Kono, Hajime
author_facet Kimura, Yoshitaka
Tsukui, Daisuke
Kono, Hajime
author_sort Kimura, Yoshitaka
collection PubMed
description Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive oxygen species (ROS) are produced simultaneously with the formation of uric acid by xanthine oxidases. Intracellular uric acid has also been reported to promote the production of ROS. The ROS and the intracellular uric acid itself regulate several intracellular signaling pathways, and alterations in these pathways may result in the development of atherosclerotic lesions. In this review, we describe the effect of uric acid on various molecular signals and the potential mechanisms of atherosclerosis development in hyperuricemia. Furthermore, we discuss the efficacy of treatments for hyperuricemia to protect against the development of atherosclerosis.
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spelling pubmed-86246332021-11-27 Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis Kimura, Yoshitaka Tsukui, Daisuke Kono, Hajime Int J Mol Sci Review Hyperuricemia is a common metabolic syndrome. Elevated uric acid levels are risk factors for gout, hypertension, and chronic kidney diseases. Furthermore, various epidemiological studies have also demonstrated an association between cardiovascular risks and hyperuricemia. In hyperuricemia, reactive oxygen species (ROS) are produced simultaneously with the formation of uric acid by xanthine oxidases. Intracellular uric acid has also been reported to promote the production of ROS. The ROS and the intracellular uric acid itself regulate several intracellular signaling pathways, and alterations in these pathways may result in the development of atherosclerotic lesions. In this review, we describe the effect of uric acid on various molecular signals and the potential mechanisms of atherosclerosis development in hyperuricemia. Furthermore, we discuss the efficacy of treatments for hyperuricemia to protect against the development of atherosclerosis. MDPI 2021-11-17 /pmc/articles/PMC8624633/ /pubmed/34830282 http://dx.doi.org/10.3390/ijms222212394 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kimura, Yoshitaka
Tsukui, Daisuke
Kono, Hajime
Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title_full Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title_fullStr Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title_full_unstemmed Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title_short Uric Acid in Inflammation and the Pathogenesis of Atherosclerosis
title_sort uric acid in inflammation and the pathogenesis of atherosclerosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8624633/
https://www.ncbi.nlm.nih.gov/pubmed/34830282
http://dx.doi.org/10.3390/ijms222212394
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