Evidence map›Paper›PMID 32914384›Full record

ArticleIn vitro cellular & developmental biology. Animal2020

Upregulation of miR-223 abrogates NLRP3 inflammasome-mediated pyroptosis to attenuate oxidized low-density lipoprotein (ox-LDL)-induced cell death in human vascular endothelial cells (ECs).

Xumin Wang, Xinwei Li, Yuhong Wu, Yuan Song

Abstract read
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In one paragraph

Article in In vitro cellular & developmental biology. Animal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Role of NLRP3 inflammasome in systemic sclerosis.Arthritis research & therapy · 2022
    Review
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Therapeutic Potential of Carbon Monoxide (CO) and Hydrogen Sulfide (HInternational journal of molecular sciences · 2020
    Review
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

4 authors at 1 institution in 1 country.

Xumin WangDepartment of Cardiovascular Medicine, Affiliated Sixth Hospital of Xinjiang Medical University, Wuxing South Road 39, Urumqi, 830000, Xinjiang, China.
Xinwei LiDepartment of Cardiovascular Medicine, Changji Branch, Affiliated First Hospital of Xinjiang Medical University, Qingnian South Road 73, Changji, 831100, Xinjiang, China.
Yuhong WuDepartment of Cardiovascular Medicine, Affiliated Sixth Hospital of Xinjiang Medical University, Wuxing South Road 39, Urumqi, 830000, Xinjiang, China.
Yuan SongDepartment of Function Examination, Affiliated Sixth Hospital of Xinjiang Medical University, Wuxing South Road 39, Urumqi, 830000, Xinjiang, China. songyuan766@163.com.ORCID http://orcid.org/0000-0002-9031-311X
Xinjiang Medical University · CN

Funding

Special Project for Young Medical Talents of Xinjiang Uygur Autonomous Region WJWY-201966
6 · The paper itself

Abstract

MiR-223 is closely associated with pathogenesis of coronary artery disease (CAD); however, the molecular mechanisms are unclear. In the present study, the human vascular endothelial cells (ECs) were isolated from patients undergoing coronary artery bypass graft and treated with oxidized low-density lipoprotein (ox-LDL) to induce cellular CAD models in vitro. We found that ox-LDL inhibited cell proliferation and viability, and promoted cell apoptosis in ECs. Of note, ox-LDL promoted cell pyroptosis, and both the pyroptosis inhibitor necrosulfonamide (NSA) and NLRP3 ablation restored cell viability in ECs treated with ox-LDL, indicating that ox-LDL induced EC death by triggering cell pyroptosis. In addition, miR-223 was downregulated by ox-LDL in ECs, and miR-223 overexpression rescued cell viability in ECs treated with ox-LDL. Interestingly, there existed targeting sites in miR-223 and 3' untranslated regions (3' UTRs) of NLRP3 mRNA, and further experiments validated that miR-223 negatively regulated NLRP3 expressions in ECs at both transcriptional and translational levels. Finally, we verified that upregulation of NLRP3 abrogated the protective effects of miR-223 overexpression on ox-LDL-treated ECs. Collectively, this in vitro study proved that overexpression of miR-223 protected ox-LDL-stimulated ECs from death through inactivating NLRP3 inflammasome-mediated pyroptotic cell death.

Indexed as

AcrylamidesApoptosisBase SequenceCell ProliferationCell SurvivalCoronary Artery DiseaseEndothelial CellsHEK293 CellsHumansInflammasomesLipoproteins, LDLMicroRNAsModels, BiologicalNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisSulfonamidesAcrylamidesInflammasomesLipoproteins, LDLMicroRNAsMIR223, humanN-(4-(N-(3-methoxypyrazin-2-yl)sulfamoyl)phenyl)-3-(5-nitrothiophene-2-yl)acrylamideNLR Family, Pyrin Domain-Containing 3 Proteinoxidized low density lipoproteinSulfonamidesCell pyroptosisCoronary artery diseaseMiR-223NLRP3Oxidized low-density lipoprotein

Identifiers

PMID32914384
OpenAlexW3086651835

What OpenQuestion holds

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Read underepoch 390

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.