Evidence map›Paper›PMID 34363750›Full record

ArticleImmunity2021

Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation.

Natalia Reglero-Real, Lorena Pérez-Gutiérrez, Azumi Yoshimura, Loïc Rolas, José Garrido-Mesa, Anna Barkaway, Catherine Pickworth, Rebeca S Saleeb, Maria Gonzalez-Nuñez, Shani N Austin-Williams and 15 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 2 pooled it
11.1field-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

62 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.

  1. Colchicine for the primary prevention of cardiovascular events.The Cochrane database of systematic reviews · 2025
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2 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

25 authors at 7 institutions in 4 countries.

Natalia Reglero-RealCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK. Electronic address: n.reglero@qmul.ac.uk.
Lorena Pérez-GutiérrezCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Azumi YoshimuraElectron Microscopy Science Technology Platform, Francis Crick Institute, London NW1 1AT, UK.
Loïc RolasCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
José Garrido-MesaCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Anna BarkawayCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Catherine PickworthCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Rebeca S SaleebCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Maria Gonzalez-NuñezCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Shani N Austin-WilliamsCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Dianne CooperCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Centre for Inflammation and Therapeutic Innovation, Queen Mary University of London, London EC1M 6BQ, UK.
Laura Vázquez-MartínezCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Tao FuDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Giulia De RossiDepartment of Cell Biology, Institute of Ophthalmology, University College London, London EC1V9EL, UK.
Matthew GoldingCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Mathieu-Benoit VoisinCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Chantal M BoulangerUniversité de Paris, PARCC, INSERM, 75015 Paris, France.
Yoshiaki KubotaDepartment of Anatomy, Keio University School of Medicine, Tokyo 113-0022, Japan.
William A MullerDepartment of Pathology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Sharon A ToozeMolecular Cell Biology of Autophagy Laboratory, Francis Crick Institute, London NW1 1AT, UK.
Thomas D NightingaleCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Lucy CollinsonElectron Microscopy Science Technology Platform, Francis Crick Institute, London NW1 1AT, UK.
Mauro PerrettiCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Centre for Inflammation and Therapeutic Innovation, Queen Mary University of London, London EC1M 6BQ, UK.
Ezra AksoyCentre for Biochemical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK.
Sussan NoursharghCentre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London EC1M 6BQ, UK; Centre for Inflammation and Therapeutic Innovation, Queen Mary University of London, London EC1M 6BQ, UK. Electronic address: s.nourshargh@qmul.ac.uk.
Queen Mary University of London · GBWilliam Harvey Research Institute · GBThe Francis Crick Institute · GBNorthwestern University · USKeio University · JPParis Cardiovascular Research Center · FRUniversity College London · GB

Funding

British Heart Foundation PG/19/60/34585Cancer Research UK FC001187Medical Research Council MR/M023230/1Wellcome Trust FC001187Wellcome Trust FC001999
6 · The paper itself

Abstract

The migration of neutrophils from the blood circulation to sites of infection or injury is a key immune response and requires the breaching of endothelial cells (ECs) that line the inner aspect of blood vessels. Unregulated neutrophil transendothelial cell migration (TEM) is pathogenic, but the molecular basis of its physiological termination remains unknown. Here, we demonstrated that ECs of venules in inflamed tissues exhibited a robust autophagic response that was aligned temporally with the peak of neutrophil trafficking and was strictly localized to EC contacts. Genetic ablation of EC autophagy led to excessive neutrophil TEM and uncontrolled leukocyte migration in murine inflammatory models, while pharmacological induction of autophagy suppressed neutrophil infiltration into tissues. Mechanistically, autophagy regulated the remodeling of EC junctions and expression of key EC adhesion molecules, facilitating their intracellular trafficking and degradation. Collectively, we have identified autophagy as a modulator of EC leukocyte trafficking machinery aimed at terminating physiological inflammation.

Indexed as

AnimalsAutophagyChemotaxis, LeukocyteEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsInflammationIntercellular JunctionsMiceMice, Inbred C57BLNeutrophil InfiltrationNeutrophilsTransendothelial and Transepithelial MigrationATG16L1ATG5autophagydiapedesisendotheliumextravasationinflammationjunctionsneutrophilsPECAM-1

Identifiers

PMID34363750
PMCPMC8459396
OpenAlexW3191515437

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.