Evidence map›Paper›PMID 35427166›Full record

ArticleScience advances2022

Pressure and stiffness sensing together regulate vascular smooth muscle cell phenotype switching.

Pamela Swiatlowska, Brian Sit, Zhen Feng, Emilie Marhuenda, Ioannis Xanthis, Simona Zingaro, Matthew Ward, Xinmiao Zhou, Qingzhong Xiao, Cathy Shanahan and 3 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
5.7field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  11. Current updates on latest basic research of scientific relevance in hypertensive dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
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  16. Article
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  18. DysregulatedLife science alliance · 2025
    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

13 authors at 3 institutions in 2 countries.

Pamela SwiatlowskaSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.ORCID 0000-0002-3705-7495
Brian SitSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.ORCID 0000-0002-9872-7202
Zhen FengSchool of Biomedical Sciences, Hong Kong University, Hong Kong, Hong Kong.ORCID 0000-0002-3064-1752
Emilie MarhuendaSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.ORCID 0000-0003-2357-9505
Ioannis XanthisSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Simona ZingaroRandall Centre for Cell and Molecular Biophysics, King's College London, London, UK.
Matthew WardSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.
Xinmiao ZhouWilliam Harvey Research Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-2235-0338
Qingzhong XiaoWilliam Harvey Research Institute, Queen Mary University of London, London, UK.ORCID 0000-0001-9101-0498
Cathy ShanahanSchool of Cardiovascular Medicine and Sciences, King's College London, London, UK.ORCID 0000-0002-8352-8171
Gareth E JonesRandall Centre for Cell and Molecular Biophysics, King's College London, London, UK.
Cheng-Han YuSchool of Biomedical Sciences, Hong Kong University, Hong Kong, Hong Kong.ORCID 0000-0002-8821-8877
Thomas IskratschSchool of Engineering and Materials Science, Queen Mary University of London, London, UK.ORCID 0000-0002-3738-7830
Queen Mary University of London · GBKing's College London · GBUniversity of Hong Kong · HK

Funding

British Heart Foundation FS/14/30/30917British Heart Foundation PG/20/10458
6 · The paper itself

Abstract

Vascular smooth muscle cells (VSMCs) play a central role in the progression of atherosclerosis, where they switch from a contractile to a synthetic phenotype. Because of their role as risk factors for atherosclerosis, we sought here to systematically study the impact of matrix stiffness and (hemodynamic) pressure on VSMCs. Thereby, we find that pressure and stiffness individually affect the VSMC phenotype. However, only the combination of hypertensive pressure and matrix compliance, and as such mechanical stimuli that are prevalent during atherosclerosis, leads to a full phenotypic switch including the formation of matrix-degrading podosomes. We further analyze the molecular mechanism in stiffness and pressure sensing and identify a regulation through different but overlapping pathways culminating in the regulation of the actin cytoskeleton through cofilin. Together, our data show how different pathological mechanical signals combined but through distinct pathways accelerate a phenotypic switch that will ultimately contribute to atherosclerotic disease progression.

Indexed as

AtherosclerosisMuscle, Smooth, VascularCell ProliferationCells, CulturedHumansPhenotype

Identifiers

PMID35427166
PMCPMC9012473
OpenAlexW4223977830

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.