Evidence map›Paper›PMID 28539647›Full record

ArticleScientific reports2017

Physiological concentrations of soluble uric acid are chondroprotective and anti-inflammatory.

Jenn-Haung Lai, Shue-Fen Luo, Li-Feng Hung, Chuan-Yueh Huang, Shiu-Bii Lien, Leou-Chyr Lin, Feng-Cheng Liu, B Linju Yen, Ling-Jun Ho

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 52 citations in OpenAlex.

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  15. Hyperuricemia-induced endothelial insulin resistance: the nitric oxide connection.Pflugers Archiv : European journal of physiology · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Jenn-Haung LaiDepartment of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, Lin-Kou, Tao-Yuan, Taiwan, ROC.
Shue-Fen LuoDepartment of Rheumatology, Allergy and Immunology, Chang Gung Memorial Hospital, Lin-Kou, Tao-Yuan, Taiwan, ROC.
Li-Feng HungInstitute of Cellular and System Medicine, National Health Research Institute, Zhunan, Taiwan, ROC.
Chuan-Yueh HuangInstitute of Cellular and System Medicine, National Health Research Institute, Zhunan, Taiwan, ROC.
Shiu-Bii LienDepartment of Orthopaedics, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Leou-Chyr LinDepartment of Orthopaedics, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
Feng-Cheng LiuRheumatology/Immunology and Allergy, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
B Linju YenInstitute of Cellular and System Medicine, National Health Research Institute, Zhunan, Taiwan, ROC.
Ling-Jun HoInstitute of Cellular and System Medicine, National Health Research Institute, Zhunan, Taiwan, ROC. lingjunho@nhri.org.tw.
National Health Research Institutes · TWNational Defense Medical Center · TWChang Gung Memorial Hospital · TWTri-Service General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High uric acid levels are a risk factor for cardiovascular disorders and gout; however, the role of physiological concentrations of soluble uric acid (sUA) is poorly understood. This study aimed to clarify the effects of sUA in joint inflammation. Both cell cultures of primary porcine chondrocytes and mice with collagen-induced arthritis (CIA) were examined. We showed that sUA inhibited TNF-α- and interleukin (IL)-1β-induced inducible nitric oxide synthase, cyclooxygenase-2 and matrix metalloproteinase (MMP)-13 expression. Examination of the mRNA expression of several MMPs and aggrecanases confirmed that sUA exerts chondroprotective effects by inhibiting the activity of many chondro-destructive enzymes. These effects attenuated collagen II loss in chondrocytes and reduced proteoglycan degradation in cartilage explants. These results were reproduced in chondrocytes cultured in three-dimensional (3-D) alginate beads. Molecular studies revealed that sUA inhibited the ERK/AP-1 signalling pathway, but not the IκBα-NF-κB signalling pathway. Increases in plasma uric acid levels facilitated by the provision of oxonic acid, a uricase inhibitor, to CIA mice exerted both anti-inflammatory and arthroprotective effects in these animals, as demonstrated by their arthritis severity scores and immunohistochemical analysis results. Our study demonstrated that physiological concentrations of sUA displayed anti-inflammatory and chondroprotective effects both in vitro and in vivo.

Indexed as

AnimalsAnti-Inflammatory AgentsArthritis, ExperimentalCartilage, ArticularCells, CulturedChondrocytesCyclooxygenase 2Gene Expression Regulation, EnzymologicInterleukin-1betaMaleMatrix Metalloproteinase 13Mice, Inbred DBANitric Oxide Synthase Type IIProtective AgentsSignal TransductionSolubilityAnti-Inflammatory AgentsCyclooxygenase 2Interleukin-1betaMatrix Metalloproteinase 13Nitric Oxide Synthase Type IIProtective AgentsTumor Necrosis Factor-alphaUric Acid

Identifiers

PMID28539647
PMCPMC5443811
OpenAlexW2614861673

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.