Evidence map›Paper›PMID 30052471›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2018

Atheroprone flow enhances the endothelial-to-mesenchymal transition.

Baochang Lai, Zhao Li, Ming He, Yili Wang, Lili Chen, Jiao Zhang, Yan Yang, John Y-J Shyy

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
3.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

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  14. Vascular mechanotransduction.Physiological reviews · 2023
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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

8 authors at 3 institutions in 2 countries.

Baochang LaiThe Key Laboratory of Biomedical Information Engineering, Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University , Xi'an, Shaanxi China.
Zhao LiCardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi , China.
Ming HeDivision of Cardiology, Department of Medicine, University of California, San Diego, La Jolla, California.
Yili WangThe Key Laboratory of Biomedical Information Engineering, Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University , Xi'an, Shaanxi China.
Lili ChenCardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi , China.
Jiao ZhangDivision of Cardiology, Department of Medicine, University of California, San Diego, La Jolla, California.
Yan YangDepartment of Obstetrics and Gynaecology, the First Affiliated Hospital of Xi'an Jiaotong University , Xi'an, Shaanxi China.
John Y-J ShyyCardiovascular Research Center, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center , Xi'an, Shaanxi , China.
Xi'an Jiaotong University · CNUniversity of California San Diego · USFirst Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

Flow-Induced Endothelial Innate Immunity and Atherosclerosis SusceptibilityR01HL125643 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHYY, JOHN YJ · 2016 to 2019
$1.7M
NHLBI NIH HHS R01 HL125643
6 · The paper itself

Abstract

The endothelial-to-mesenchymal transition (EndoMT) is a cellular process featuring decreased expression of endothelial marker genes but increased expression of mesenchymal marker genes. The EndoMT is involved in endothelial dysfunction and the pathogenesis of atherosclerosis. To investigate the dynamic expression of EndoMT genes in vascular endothelial cells under atheroprotective pulsatile shear stress (PS) and atheroprone oscillatory shear stress (OS), we analyzed RNA sequencing data from multitimepoint shear-stress experiments. This unbiased analysis involving next-generation sequencing confirmed that PS and OS had an opposite effect in regulating EndoMT genes. Further experimental validations with H

Indexed as

Epithelial-Mesenchymal TransitionPulsatile FlowAMP-Activated Protein KinasesAnimalsAntigens, CDAtherosclerosisAtorvastatinCadherin 5CadherinsCells, CulturedDNA MethylationEpigenesis, GeneticGene Expression RegulationHumansHuman Umbilical Vein Endothelial CellsMetforminAMP-Activated Protein KinasesAntigens, CDAtorvastatinCadherin 5CadherinsCDH2 protein, humanMetforminPlatelet Endothelial Cell Adhesion Molecule-1S100A4 protein, humanS100 Calcium-Binding Protein A4SIRT1 protein, humanSirtuin 1VimentinVIM protein, humanvon Willebrand FactorAMP-activated protein kinaseendothelial-to-mesenchymal transitionendotheliumshear stresssirtuin 1

Identifiers

PMID30052471
PMCPMC6297807
OpenAlexW2884409188

What OpenQuestion holds

Texttitle and abstract
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.