Evidence map›Paper›PMID 36585554›Full record

ArticleCardiovascular drugs and therapy2024

Circ_0026218 ameliorates oxidized low-density lipoprotein-induced vascular endothelial cell dysfunction by regulating miR-188-3p/TLR4/NF-κB pathway.

Jing Liu, Xiangyang Zhang, Zhaoxia Yu, Tieliang Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Cardiovascular drugs and therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  7. Article
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  11. Circular RNAs Variously Participate in Coronary Atherogenesis.Current issues in molecular biology · 2023
    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

4 authors at 1 institution in 1 country.

Jing LiuDepartments of coronary heart disease, First Affiliated Hospital of Xinjiang Medical University, Urumqi City, China.
Xiangyang ZhangDepartments of coronary heart disease, Xinjiang Medical University, Urumqi City, China.
Zhaoxia YuCritical Care Medicine, First Affiliated Hospital of Xinjiang Medical University, Urumqi City, China.
Tieliang ZhangImage Center, First Affiliated Hospital of Xinjiang Medical University, 137 Liushan South Road, Urumqi City, 830000, Xinjiang Province, China. xclj8355@163.com.ORCID 0000-0002-8063-1237
Xinjiang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCircular RNAs (circRNAs) have shown important regulatory roles in cardiovascular diseases, including atherosclerosis (AS). However, the role and mechanism of circ_0026218 in AS remain unclear.

methodsThe cell model of AS in vitro was established by stimulating human umbilical vein endothelial cells (HUVECs) with oxidized low-density lipoprotein (ox-LDL). In addition, circ_0026218, microRNA-188-3p (miR-188-3p), and toll-like receptor 4 (TLR4) expression was determined via real-time quantitative polymerase chain reaction (RT-qPCR) in serum samples from AS patients and healthy volunteers. Cell proliferation was assessed using Cell Counting Kit-8 (CCK-8) assay and 5-ethynyl-2'-deoxyuridine (EdU) assay. Cell apoptosis was measured using flow cytometry. The inflammatory response was assessed using enzyme-linked immunosorbent assay (ELISA). Oxidative stress level was assessed using corresponding kits. Nitric oxide (NO) level was examined using NO detection assay. The interaction between miR-188-3p and circ_0026218 or TLR4 was determined via dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays. Exosomes were observed using transmission electron microscopy (TEM). The size distribution of exosomes was analyzed using nanoparticle tracking analysis (NTA).

resultsOx-LDL treatment caused HUVEC dysfunction by inhibiting cell proliferation and promoting apoptosis, inflammation, and oxidative stress. Circ_0026218 was upregulated in AS serum samples and ox-LDL-treated HUVECs. Knockdown of circ_0026218 attenuated ox-LDL-induced dysfunction in HUVECs. MiR-188-3p acted as a target of circ_0026218, and miR-188-3p downregulation reversed the suppression role of circ_0026218 knockdown on ox-LDL-induced HUVEC disorder. TLR4 was a target of miR-188-3p, and miR-188-3p overexpression alleviated ox-LDL-induced dysfunction in HUVECs by targeting TLR4. Circ_0026218 could deregulate the TLR4/NF-κB pathway by sponging the miR-188-3p. Importantly, circ_0026218 was overexpressed in exosomes from ox-LDL-treated HUVECs and could be delivered via exosomes.

conclusionCirc_0026218 knockdown attenuated ox-LDL-induced dysfunction in HUVECs via regulating miR-188-3p/TLR4/NF-κB pathway.

Indexed as

AtherosclerosisMicroRNAsApoptosisCell ProliferationHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLNF-kappa BToll-Like Receptor 4Lipoproteins, LDLMicroRNAsMIRN188 microRNA, humanNF-kappa Boxidized low density lipoproteinTLR4 protein, humanToll-Like Receptor 4atherosclerosiscirc_0026218exosomemiR-188-3pNF-κBTLR4

Identifiers

PMID36585554
OpenAlexW4313340343

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.