Evidence map›Paper›PMID 33110060›Full record

ArticleNature communications2020

Modeling early stage atherosclerosis in a primary human vascular microphysiological system.

Xu Zhang, Muath Bishawi, Ge Zhang, Varun Prasad, Ellen Salmon, Jason J Breithaupt, Qiao Zhang, George A Truskey

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
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  17. Linking homocysteine and ferroptosis in cardiovascular disease: insights and implications.Apoptosis : an international journal on programmed cell death · 2024
    Review
  18. Review
  19. 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

8 authors at 3 institutions in 2 countries.

Xu ZhangDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
Muath BishawiDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.ORCID 0000-0002-8906-3600
Ge ZhangDepartment of Immunology, College of Basic Medical Science, Dalian Medical University, 116044, Dalian, China.
Varun PrasadDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
Ellen SalmonDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
Jason J BreithauptDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
Qiao ZhangDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA.
George A TruskeyDepartment of Biomedical Engineering, Duke University, Durham, NC, 27708, USA. gtruskey@duke.edu.ORCID 0000-0002-6885-4489
Duke University · USUniversity of Miami · USUniversity of North Carolina at Chapel Hill · US

Funding

In Vitro Human Tissue-Engineered Blood Vessel Disease Model of ProgeriaR01HL138252 · NHLBI · DUKE UNIVERSITY · PI TRUSKEY, GEORGE A · 2017 to 2025
$4.7M
Vascular, Cardiac, and Lung Alveolar Human Microphysiological Systems for SARS-CoV-2 Drug ScreeningUH3TR002142 · NCATS · DUKE UNIVERSITY · PI TRUSKEY, GEORGE A · 2019 to 2021
$4.0M
Stimulating Access to Research in Residency (StARR) - NHLBIR38HL143612 · NHLBI · DUKE UNIVERSITY · PI Mai ElMallah, David H. Harpole · 2018 to 2026
$2.6M
Systemic Inflammation in Microphysiological Models of Muscle and Vascular DiseaseUG3TR002142 · NCATS · DUKE UNIVERSITY · PI TRUSKEY, GEORGE A · 2017 to 2018
$2.1M
NCATS NIH HHS UG3 TR002142NCATS NIH HHS UH3 TR002142NHLBI NIH HHS R01 HL138252NHLBI NIH HHS R38 HL143612
6 · The paper itself

Abstract

Novel atherosclerosis models are needed to guide clinical therapy. Here, we report an in vitro model of early atherosclerosis by fabricating and perfusing multi-layer arteriole-scale human tissue-engineered blood vessels (TEBVs) by plastic compression. TEBVs maintain mechanical strength, vasoactivity, and nitric oxide (NO) production for at least 4 weeks. Perfusion of TEBVs at a physiological shear stress with enzyme-modified low-density-lipoprotein (eLDL) with or without TNFα promotes monocyte accumulation, reduces vasoactivity, alters NO production, which leads to endothelial cell activation, monocyte accumulation, foam cell formation and expression of pro-inflammatory cytokines. Removing eLDL leads to recovery of vasoactivity, but not loss of foam cells or recovery of permeability, while pretreatment with lovastatin or the P2Y

Indexed as

ArteriolesAtherosclerosisBiomechanical PhenomenaCell AdhesionCell ProliferationCells, CulturedFoam CellsHumansLipoproteins, LDLModels, BiologicalMonocytesNitric OxideTissue EngineeringTumor Necrosis Factor-alphaLipoproteins, LDLNitric OxideTumor Necrosis Factor-alpha

Identifiers

PMID33110060
PMCPMC7591486
OpenAlexW3095202503

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.