Evidence map›Paper›PMID 34851051›Full record

ArticlePhysiological reports2021

CFTR limits F-actin formation and promotes morphological alignment with flow in human lung microvascular endothelial cells.

Adam J Causer, Maha Khalaf, Emily Klein Rot, Kimberly Brand, James Smith, Stephen J Bailey, Michael H Cummings, Anthony I Shepherd, Zoe L Saynor, Janis K Shute

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. CFTR as a therapeutic target for severe lung infection.American journal of physiology. Lung cellular and molecular physiology · 2025
    Review
  2. CFTR dictates monocyte adhesion by facilitating integrin clustering but not activation.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
  4. Article
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

10 authors at 5 institutions in 2 countries.

Adam J CauserDepartment for Health, University of Bath, Bath, UK.
Maha KhalafSchool of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.
Emily Klein RotSchool of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.
Kimberly BrandSchool of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.
James SmithSchool of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.
Stephen J BaileySchool of Sport, Exercise and Health Sciences, Loughborough University, Loughborough, UK.
Michael H CummingsDepartment of Diabetes and Endocrinology, Queen Alexandra Hospital, Portsmouth, UK.
Anthony I ShepherdSchool of Sport, Health and Exercise Science, University of Portsmouth, Portsmouth, UK.
Zoe L SaynorSchool of Sport, Health and Exercise Science, University of Portsmouth, Portsmouth, UK.
Janis K ShuteSchool of Pharmacy and Biomedical Sciences, University of Portsmouth, Portsmouth, UK.ORCID 0000-0002-6586-7583
University of Portsmouth · GBSaxion · NLLoughborough University · GBQueen Alexandra Hospital · GBUniversity of Bath · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Micro- and macrovascular endothelial dysfunction in response to shear stress has been observed in cystic fibrosis (CF), and has been associated with inflammation and oxidative stress. We tested the hypothesis that the cystic fibrosis transmembrane conductance regulator (CFTR) regulates endothelial actin cytoskeleton dynamics and cellular alignment in response to flow. Human lung microvascular endothelial cells (HLMVEC) were cultured with either the CFTR inhibitor GlyH-101 (20 µM) or CFTRinh-172 (20 µM), tumor necrosis factor (TNF)-α (10 ng/ml) or a vehicle control (0.1% dimethyl sulfoxide) during 24 and 48 h of exposure to shear stress (11.1 dynes/cm

Indexed as

Actin CytoskeletonActinsCystic Fibrosis Transmembrane Conductance RegulatorEndothelial CellsEndothelin-1GlycineHumansHydrazinesLungNitritesStress, MechanicalTumor Necrosis Factor-alphaActinsCystic Fibrosis Transmembrane Conductance RegulatorEndothelin-1GlycineHydrazinesN-(2-naphthalenyl)-((3,5-dibromo-2,4-dihydroxyphenyl)methylene)glycine hydrazideNitritesTumor Necrosis Factor-alphaactin cytoskeletoncystic fibrosispulmonary microvascular endotheliumshear stress

Identifiers

PMID34851051
PMCPMC8634629
OpenAlexW3211344702

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.