Evidence map›Paper›PMID 32695290›Full record

ArticleIranian journal of basic medical sciences2020

Soluble uric acid induces inflammation via TLR4/NLRP3 pathway in intestinal epithelial cells.

Chunling Ma, Xiaomin Yang, Qiulan Lv, Zhimei Yan, Zeqing Chen, Daxing Xu, Xiu Liu, Wan Yang, Shichao Xing

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Supplementation ofNutrients · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Uric acid drives intestinal barrier dysfunction through TSPO-mediated NLRP3 inflammasome activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
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 1 institution in 1 country.

Chunling MaMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Xiaomin YangMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Qiulan LvMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Zhimei YanMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Zeqing ChenMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Daxing XuMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Xiu LiuMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Wan YangMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
Shichao XingMedical Research Center, the Affiliated Hospital of Qingdao University, Qingdao, Shandong Province, 266000, P. R. China.
King's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesHyperuricemia is a risk for cardiovascular and metabolic diseases, but the mechanism is ambiguous. Increased intestinal permeability is correlated with metabolic syndrome risk factors. Intestinal epithelial cells play a pivotal role in maintaining intestinal permeability. Uric acid is directly eliminated into intestinal lumen, however, the mechanism and effect of uric acid on intestinal epithelial cells is poorly explored. Here we carried out an analysis to identify the effect and mechanism of uric acid on intestinal epithelial cells. MATERIALS AND

methodsIEC-6 was exposed to different concentrations of uric acid to simulate the effect of uric acid on intestinal epithelial cells. Cell viability was determined by MTS assay. Protein content and mRNA were assessed using Western blotting and Q-PCR, respectively. Intracellular ROS was determined using flow-cytometry and fluorescence microscopy. Mitochondrial membrane potential was detected by immunofluorescence using a mitochondrial membrane potential assay kit with JC-1. Small interfering RNA transfection was used to suppress the expression of TLR4.

resultsWe found soluble uric acid alone increased the release of ROS, depolarized the mitochondrial membrane potential, up-regulated TSPO, increased the expression of TLR4 and NLRP3, and then activated NLRP3 inflammasome and NF-κB signaling, which further resulted in lower expression of tight junction protein and exerted adverse effects on intestinal epithelial cells. Furthermore, the elevated IL-1β could be restored by silencing of TLR4, indicating soluble uric acid induces inflammation via the TLR4/NLRP3 pathway.

conclusionSoluble uric acid exerted detrimental effect on intestinal epithelial cells through the TLR4/NLRP3 pathway.

Indexed as

HyperuricemiaInflammasomeIntestinal epitheliumMechanismROS

Identifiers

PMID32695290
PMCPMC7351448
OpenAlexW3027608027

What OpenQuestion holds

Textmetadata
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.