Evidence map›Paper›PMID 30690853›Full record

ArticleThe FEBS journal2019

Urate-lowering therapy alleviates atherosclerosis inflammatory response factors and neointimal lesions in a mouse model of induced carotid atherosclerosis.

Jie Lu, Mingshu Sun, Xinjiang Wu, Xuan Yuan, Zhen Liu, Xiaojie Qu, Xiaopeng Ji, Tony R Merriman, Changgui Li

Open access · hybridAbstract read
In one paragraph

Article in The FEBS journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
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  7. Article
  8. Novel Insights into the Molecular Mechanisms of Atherosclerosis.International journal of molecular sciences · 2023
    Review
  9. Review
  10. Do thrifty genes exist? Revisiting uricase.Obesity (Silver Spring, Md.) · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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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 3 countries.

Jie LuInstitute of Metabolic Diseases, Qingdao University, China.
Mingshu SunInstitute of Metabolic Diseases, Qingdao University, China.
Xinjiang WuInstitute of Metabolic Diseases, Qingdao University, China.
Xuan YuanInstitute of Metabolic Diseases, Qingdao University, China.
Zhen LiuInstitute of Metabolic Diseases, Qingdao University, China.
Xiaojie QuInstitute of Metabolic Diseases, Qingdao University, China.
Xiaopeng JiInstitute of Metabolic Diseases, Qingdao University, China.
Tony R MerrimanDepartment of Biochemistry, University of Otago, Dunedin, New Zealand.
Changgui LiInstitute of Metabolic Diseases, Qingdao University, China.
Institut des Maladies Métaboliques et Cardiovasculaires · FRAffiliated Hospital of Qingdao University · CNQingdao University · CNUniversity of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyperuricemia (HU) is a cause of gout. Clinical studies show a link between HU and cardiovascular disease. However, the role of soluble serum urate (SU) on atherosclerosis development remains elusive. We aimed to use a new HU mouse model [Uricase/Uox knockout (KO)] to further investigate the relationship between HU and atherosclerosis. A mouse model by perivascular collar placement of induced carotid atherosclerosis was established in male Uox-KO mice. The Uox-KO mice had elevated SU levels and enhanced levels of atherosclerosis inflammatory response proteins. In contrast, Uox-KO mice with carotid atherosclerosis showed severe neointimal changes in histology staining consistent with increases in intimal area and increases in proliferating cell nuclear antigen (PCNA)- and F4/80-positive cells. Allopurinol reduced neointimal areas induced by the perivascular collar in hyperuricemic mice, accompanied by decreased expression of PCNA- and F4/80-positive cells. Urate-lowering treatment alleviated atherosclerosis inflammatory response factors and reactive oxygen species (ROS) intensities in both collar placement Uox-KO mice and urate-stimulated human umbilical vein endothelial cells (HUVECs). In vitro results using HUVECs showed ROS was induced by urate and ROS induction was abrogated using antioxidants. These data demonstrate that urate per se does not trigger atherosclerosis intima lesions in male mice. Urate worsens carotid neointimal lesions induced by the perivascular collar and urate-lowering therapy partially abrogates the effects. The current study warrants clinical studies on the possible benefits of urate-lowering therapy in atherosclerosis patients with HU.

Indexed as

AllopurinolAnimalsAntimetabolitesCarotid Artery DiseasesHumansHuman Umbilical Vein Endothelial CellsHyperuricemiaInflammationMaleMiceMice, Inbred C57BLMice, KnockoutNeointimaReactive Oxygen SpeciesUrate OxidaseUric AcidAllopurinolAntimetabolitesReactive Oxygen SpeciesUrate OxidaseUric Acidallopurinolanimal modelatherosclerosisreactive oxygen speciesurate

Identifiers

PMID30690853
PMCPMC6849826
OpenAlexW2911465583

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.