Evidence map›Paper›PMID 29507690›Full record

ArticleOncotarget2018

Chronic hyperuricemia impairs blood flow recovery in the ischemic hindlimb through suppression of endothelial progenitor cells.

I-Chun Chen, Chin-Sung Kuo, Chih-Cheng Wu, Hsiao-Ya Tsai, Chih-Pei Lin, Szu-Yuan Li, Ruey-Hsing Chou, Po-Hsun Huang, Jaw-Wen Chen, Shing-Jong Lin

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
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Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 10 citations in OpenAlex.

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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

10 authors at 4 institutions in 1 country.

I-Chun ChenInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Chin-Sung KuoInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Chih-Cheng WuCardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan.
Hsiao-Ya TsaiInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Chih-Pei LinDepartment of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
Szu-Yuan LiInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Ruey-Hsing ChouInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Po-Hsun HuangInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
Jaw-Wen ChenCardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan.
Shing-Jong LinInstitute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan.
National Yang Ming Chiao Tung University · TWNational Yang Ming University Hospital · TWNational Tsing Hua University · TWTaipei Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveChronic hyperuricemia is associated with cardiovascular disease, but its impact on endothelial progenitor cells (EPC) and ischemia-induced neovascularization remains unclear. Herein we investigated whether chronic hyperuricemia could impede blood flow recovery in response to tissue ischemia by suppression of EPC.

methodsHuman EPC were isolated and cultured in a high-level uric acid medium for functional testing. Cell proliferation, nitric oxide (NO) production and apoptosis assay were examined. A chronic hyperuricemia mouse model was established by potassium oxonate treatment and/or a high-level uric acid diet to evaluate the actions of chronic hyperuricemia on ischemia-induced blood flow recovery. After 4 weeks of drug treatment, hindlimb ischemia surgery was performed in the control and hyperuricemia mice. Blood flow recovery was followed up every week before and after ischemic surgery using a laser Doppler Perfusion Imager System. The circulating EPC number in the peripheral blood was determined by flow cytometry (Sca-1

resultsIncubation with a high-level uric acid medium (10 mg/dL) significantly suppressed EPC proliferation, reduced NO production, and lessened phosphorylation of Akt and eNOS. Moreover, EPC treated with high-level uric acid increased reactive oxygen species production, promoted cellular apoptosis and senescence, and also inhibited EPC tube formation. Four weeks after hindlimb ischemia surgery, the chronic hyperuricemia mice had significantly reduced tissue reperfusion, EPC mobilization, and impaired neovascularization in the ischemic hindlimbs compared with the control mice.

conclusionsChronic hyperuricemia impaired blood flow recovery and EPC mobilization in response to tissue ischemia, and these effects could have occurred through suppression of EPC.

Indexed as

endothelial progenitor cellhyperuricemiaischemianeovascularization

Identifiers

PMID29507690
PMCPMC5823617
OpenAlexW2791859505

What OpenQuestion holds

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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.