Evidence map›Paper›PMID 41420380›Full record

ArticlePhysiological reports2025

The role of aging on endothelial cell-cell junctions and pulmonary microvascular permeability in male mice.

Aminmohamed Manji, Lefeng Wang, Cynthia Pape, Sanjay Mehta, Preya Patel, Samuel-Caleb Yeung, Eric K Patterson, Antoine Dufour, Daniel Young, Ruud A W Veldhuizen and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiological reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

11 authors.

Aminmohamed ManjiCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.ORCID 0009-0008-2510-892X
Lefeng WangCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.
Cynthia PapeCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.
Sanjay MehtaCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.
Preya PatelDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.
Samuel-Caleb YeungDepartment of Physiology and Pharmacology, Schulich School of Medicine and Dentistry, Western University, London, Ontario, Canada.
Eric K PattersonCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.
Antoine DufourDepartment of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Daniel YoungDepartment of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Ruud A W VeldhuizenCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.
Sean E GillCentre for Critical Illness Research, London Health Sciences Centre Research Institute, London, Ontario, Canada.ORCID 0000-0003-4791-1576

Funding

Government of Canada | Canadian Institutes of Health Research (CIHR) #PJT-185943Government of Canada | Canadian Institutes of Health Research (CIHR) #PRR-177919Government of Ontario: Ontario Graduate ScholarshipLondon Health Sciences Centre (LHSC) #IRF-12-22Western University (UWO) #50658Western University (UWO): Dean's Research Scholarship
6 · The paper itself

Abstract

Pulmonary microvascular endothelial cell (PMVEC) intercellular junctions are critical for maintaining barrier function and mitigating pulmonary edema. Previously, we demonstrated that aging exacerbated pulmonary microvascular permeability in a model of lung injury. Based on this, we hypothesized that aging was associated with increased PMVEC barrier dysfunction due to impaired cell-cell junction integrity. PMVEC were isolated from young and aged mice and cultured to confluence in vitro. Barrier function, junctional integrity, alterations in the proteome, markers of inflammation, and actin cytoskeleton organization were all assessed. To model injurious conditions, PMVEC were stimulated with inflammatory cytokines. PMVEC from aged mice exhibited increased permeability, both under basal and inflammatory conditions, which was associated with disrupted cell-surface localization of the adherens junction protein, vascular endothelial (VE)-cadherin. Protein abundance of VE-cadherin was increased with age, while levels of the adapter protein,

Indexed as

AgingCapillary PermeabilityEndothelial CellsIntercellular JunctionsLungAdherens JunctionsAnimalsAntigens, CDCadherin 5CadherinsCells, CulturedClaudin-5MaleMiceMice, Inbred C57BLAntigens, CDCadherin 5CadherinsClaudin-5agingcell–cell junctionspulmonary microvascular endothelial cellsvascular permeability

Identifiers

PMID41420380
PMCPMC12717451

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Registered trials

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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.