Evidence map›Paper›PMID 34519627›Full record

ArticleBioengineered2021

A circular RNA, circUSP36, accelerates endothelial cell dysfunction in atherosclerosis by adsorbing miR-637 to enhance WNT4 expression.

Jian-Guo Huang, Xia Tang, Jiang-Jie Wang, Jia Liu, Ping Chen, Yan Sun

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.5field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. [circ_0084043/miR-31-5p Is Involved in Atherosclerosis by Regulating HMGA1: Investigation of the Mechanisms].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024
    Article
  7. Article
  8. Article
  9. Observational
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Article
  20. 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

6 authors at 1 institution in 2 countries.

Jian-Guo HuangDepartment of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Xia TangDepartment of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Jiang-Jie WangDepartment of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Jia LiuDepartment of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Ping ChenDepartment of Vascular Surgery, Linyi Central Hospital, Linyi, Shandong Province, China.
Yan SunDepartment of Mental Health, Yishui People's Hospital, Linyi, Shandong Province, China.ORCID 0000-0002-1045-4933
Linyi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a fatal disorder that is fundamental to various cardiovascular diseases and severely threatens people's health worldwide. Several studies have demonstrated the role of circular RNAs (circRNAs) in the pathogenesis of atherosclerosis. circUSP36 acts as a key modulator in the progression of atherosclerosis, but the molecular mechanism underlying this role is as yet unclear. This study aimed to elucidate the mechanism by which circUSP36 exerts its function in an in vitro cell model of endothelial cell dysfunction, which is one of pathological features of atherosclerosis. The circRNA traits of circUSP36 were confirmed, and we observed high expression of circUSP36 in endothelial cells exposed to oxidized low-density lipoprotein (ox-LDL). Functional assays revealed that overexpression of circUSP36 suppressed proliferation and migration of ox-LDL-treated endothelial cells. In terms of its mechanism, circUSP36 adsorbed miR-637 by acting as an miRNA sponge. Moreover, enhanced expression of miR-637 abated the impact of circUSP36 on ox-LDL-treated endothelial cell dysregulation. Subsequently, the targeting relationship between miR-637 and WNT4 was predicted using bioinformatics tools and was confirmed via luciferase reporter and RNA pull-down assays. Notably, depletion of WNT4 rescued circUSP36-mediated inhibition of endothelial cell proliferation and migration. In conclusion, circUSP36 regulated WNT4 to aggravate endothelial cell injury caused by ox-LDL by competitively binding to miR-637; this finding indicates circUSP36 to be a promising biomarker for the diagnosis and therapy of atherosclerosis.

Indexed as

AtherosclerosisCells, CulturedEndothelial CellsHumansMicroRNAsRNA, CircularWnt4 ProteinMicroRNAsMIRN637 microRNA, humanRNA, CircularWnt4 ProteinWNT4 protein, humanAtherosclerosiscircRNAendothelial cellmiR-637USP36Wnt4

Identifiers

PMID34519627
PMCPMC8806706
OpenAlexW3200128704

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.