Evidence map›Paper›PMID 33510936›Full record

ArticleMolecular therapy. Nucleic acids2021

Icariin attenuates endothelial-mesenchymal transition via H19/miR-148b-3p/ELF5 in ox-LDL-stimulated HUVECs.

Shan Liu, Dong-Sheng Xu, Min Li, Yang Zhang, Qi Li, Teng-Teng Li, Li-Qun Ren

Open access · goldAbstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 23% 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, 27 citations in OpenAlex.

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  16. Role of endothelial cells in vascular calcification.Frontiers in cardiovascular medicine · 2022
    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

7 authors at 2 institutions in 1 country.

Shan LiuDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Dong-Sheng XuCancer Center, The First Hospital of Jilin University, Changchun 130021, Jilin Province, China.
Min LiDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Yang ZhangDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Qi LiDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Teng-Teng LiDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Li-Qun RenDepartment of Experimental Pharmacology and Toxicology, School of Pharmacy, Jilin University, Changchun 130021, Jilin Province, China.
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is the main cause of cardio-cerebrovascular diseases. Endothelial-mesenchymal transition plays an important role in atherosclerosis. Icariin has a protective effect on atherosclerosis; however, the underlying mechanism remains unclear. In this study, we explored the molecular mechanism underlying the protective function of icariin in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells. H19, a long non-coding RNA, was identified to be downregulated in the background of the oxidized low-density lipoprotein-induced endothelial-mesenchymal transition in human umbilical vein endothelial cells. Icariin upregulated H19 expression and inhibited the transformation of endothelial cells into interstitial cells. Overexpression of H19 affected endothelial-mesenchymal transition in oxidized low-density lipoprotein-stimulated human umbilical vein endothelial cells, whereas H19 knockdown reversed endothelial protective effects of icariin and reduced human umbilical vein endothelial cell migration. Knockdown of H19 significantly downregulated oxidized low-density lipoprotein-induced E74-like factor 5 and upregulated miR-148b-3p, which was reversed by icariin. Thus, icariin may play a protective role in atherosclerosis, and H19 may be a potential therapeutic target.

Indexed as

atherosclerosisELF5endothelial-to-mesenchymal transitionH19miR-148b-3p

Identifiers

PMID33510936
PMCPMC7809175
OpenAlexW3108719759

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.