Evidence map›Paper›PMID 31366922›Full record

ReviewNature reviews. Cardiology2020

Endothelial responses to shear stress in atherosclerosis: a novel role for developmental genes.

Celine Souilhol, Jovana Serbanovic-Canic, Maria Fragiadaki, Timothy J Chico, Victoria Ridger, Hannah Roddie, Paul C Evans

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
263citing papers in PubMed, 3 pooled it
15.8field-weighted citation impact, top 1% 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

263 citing papers in PubMed, 3 syntheses or guidelines pooled it, 465 citations in OpenAlex.

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203 more citing papers are in PubMed but not listed here.

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.

Celine Souilhol *Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Jovana Serbanovic-Canic *Department of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Maria FragiadakiDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Timothy J ChicoDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.
Victoria RidgerDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.ORCID http://orcid.org/0000-0003-4163-669X
Hannah RoddieDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK.ORCID http://orcid.org/0000-0001-9428-4697
Paul C EvansDepartment of Infection, Immunity and Cardiovascular Disease, University of Sheffield, Sheffield, UK. paul.evans@sheffield.ac.uk.ORCID http://orcid.org/0000-0001-7975-681X
University of Sheffield · GBInsigneo · GB

Funding

British Heart Foundation PG/09/087/28051British Heart Foundation PG/13/2/29902British Heart Foundation PG/15/17/31332British Heart Foundation PG/17/56/33115British Heart Foundation PG/18/63/33968British Heart Foundation RG/19/10/34506
6 · The paper itself

Abstract

Flowing blood generates a frictional force called shear stress that has major effects on vascular function. Branches and bends of arteries are exposed to complex blood flow patterns that exert low or low oscillatory shear stress, a mechanical environment that promotes vascular dysfunction and atherosclerosis. Conversely, physiologically high shear stress is protective. Endothelial cells are critical sensors of shear stress but the mechanisms by which they decode complex shear stress environments to regulate physiological and pathophysiological responses remain incompletely understood. Several laboratories have advanced this field by integrating specialized shear-stress models with systems biology approaches, including transcriptome, methylome and proteome profiling and functional screening platforms, for unbiased identification of novel mechanosensitive signalling pathways in arteries. In this Review, we describe these studies, which reveal that shear stress regulates diverse processes and demonstrate that multiple pathways classically known to be involved in embryonic development, such as BMP-TGFβ, WNT, Notch, HIF1α, TWIST1 and HOX family genes, are regulated by shear stress in arteries in adults. We propose that mechanical activation of these pathways evolved to orchestrate vascular development but also drives atherosclerosis in low shear stress regions of adult arteries.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsAtherosclerosisEndothelium, VascularGenetic Predisposition to DiseaseHumansMechanotransduction, CellularNeovascularization, PhysiologicPhenotypeRegional Blood FlowRisk FactorsStress, MechanicalVascular Remodeling

Identifiers

PMID31366922
OpenAlexW2966654380

What OpenQuestion holds

Textmetadata
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.