Evidence map›Paper›PMID 28565756›Full record

ArticleExperimental and therapeutic medicine2017

MicroRNA-98 rescues proliferation and alleviates ox-LDL-induced apoptosis in HUVECs by targeting LOX-1.

Zhibo Chen, Mian Wang, Qiong He, Zilun Li, Yang Zhao, Wenjian Wang, Jieyi Ma, Yongxin Li, Guangqi Chang

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  4. CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022
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  7. miR-92a-3p promotes ox-LDL induced-apoptosis in HUVECs via targeting SIRT6 and activating MAPK signaling pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2021
    Article
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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 3 institutions in 1 country.

Zhibo ChenDivision of Vascular Surgery, Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Mian WangDivision of Vascular Surgery, Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Qiong HeDivision of Pathology, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Zilun LiDivision of Vascular Surgery, Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Yang ZhaoDivision of Vascular Surgery, Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Wenjian WangLaboratory of General Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Jieyi MaLaboratory of General Surgery, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
Yongxin LiDepartment of Vascular Surgery, The First Affiliated Hospital of Qingdao University, Qingdao, Shandong 266000, P.R. China.
Guangqi ChangDivision of Vascular Surgery, Guangdong Engineering Laboratory for Diagnosis and Treatment of Vascular Disease, The First Affiliated Hospital of Sun Yat-Sen University, Guangzhou, Guangdong 510080, P.R. China.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CNAffiliated Hospital of Qingdao University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidized low-density lipoprotein (ox-LDL) is a major and critical mediator of atherosclerosis, and the underlying mechanism is thought to involve the ox-LDL-induced dysfunction of endothelial cells (ECs). MicroRNAs (miRNAs), which are a group of small non-coding RNA molecules that post-transcriptionally regulate the expression of target genes, have been associated with diverse cellular functions and the pathogenesis of various diseases, including atherosclerosis. miRNA-98 (miR-98) has been demonstrated to be involved in the regulation of cellular apoptosis; however, the role of miR-98 in ox-LDL-induced dysfunction of ECs and atherosclerosis has yet to be elucidated. Therefore, the present study aimed to investigate the role of miR-98 in ox-LDL-induced dysfunction of ECs and the underlying mechanism. It was demonstrated that miR-98 expression was markedly downregulated in ox-LDL-treated human umbilical vein ECs (HUVECs) and that miR-98 promoted the proliferation and alleviated apoptosis of HUVECs exposed to ox-LDL. In addition, the results demonstrated that lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) was a direct target of miR-98 in HUVECs, as indicated by a luciferase assay. The results of the present study suggested that miR-98 may inhibit the uptake of toxic ox-LDL, maintain HUVEC proliferation and protect HUVECs against apoptosis via the suppression of LOX-1.

Indexed as

apoptosishuman umbilical vein endothelial cellslectin-like oxidized low-density lipoprotein receptor 1microRNA-98proliferation

Identifiers

PMID28565756
PMCPMC5443247
OpenAlexW2594310433

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.