Evidence map›Paper›PMID 32265308›Full record

ArticleThe European respiratory journal2020

Vascular permeability in the fibrotic lung.

Clemens K Probst, Sydney B Montesi, Benjamin D Medoff, Barry S Shea, Rachel S Knipe

Open access · bronzeAbstract read
In one paragraph

Article in The European respiratory journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.7field-weighted citation impact, top 2% 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, 89 citations in OpenAlex.

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  10. CD146: a promising target in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2025
    Review
  11. Article
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  14. CD45+/ Col I+ Fibrocytes: Major source of collagen in the fibrotic lung, but not in passaged fibroblast cultures.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Article
  15. Article
  16. Article
  17. Review
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  20. Review

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

5 authors at 2 institutions in 1 country.

Clemens K ProbstDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA.
Sydney B MontesiDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA.
Benjamin D MedoffDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA.
Barry S SheaDivision of Pulmonary and Critical Care Medicine, Brown University and Rhode Island Hospital, Providence, RI, USA.
Rachel S KnipeDivision of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Boston, MA, USA.
Massachusetts General Hospital · USBrown University · US

Funding

TRAINING GRANT IN LUNG CELL &MOLECULAR BIOLOGYT32HL007874 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MEDOFF, BENJAMIN DAVID · 1997 to 2011
$4.1M
Targeting Cell-specific Functions of the Rho Kinase Pathway in Pulmonary FibrosisR01HL133153 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MCCARTHY, JASON R., MEDOFF, BENJAMIN DAVID · 2016 to 2019
$2.7M
Vascular Leak and Outcomes in IPFK23HL150331 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI MONTESI, SYDNEY · 2020 to 2024
$887k
Role and regulation of vascular permeability in pulmonary fibrosisK08HL140175 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI KNIPE, RACHEL S · 2018 to 2022
$864k
NHLBI NIH HHS K08 HL140175NHLBI NIH HHS K23 HL150331NHLBI NIH HHS R01 HL133153NHLBI NIH HHS T32 HL007874
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is thought to result from aberrant tissue repair processes in response to chronic or repetitive lung injury. The origin and nature of the injury, as well as its cellular and molecular targets, are likely heterogeneous, which complicates accurate pre-clinical modelling of the disease and makes therapeutic targeting a challenge. Efforts are underway to identify central pathways in fibrogenesis which may allow targeting of aberrant repair processes regardless of the initial injury stimulus. Dysregulated endothelial permeability and vascular leak have long been studied for their role in acute lung injury and repair. Evidence that these processes are of importance to the pathogenesis of fibrotic lung disease is growing. Endothelial permeability is increased in non-fibrosing lung diseases, but it resolves in a self-limited fashion in conditions such as bacterial pneumonia and acute respiratory distress syndrome. In progressive fibrosing diseases such as IPF, permeability appears to persist, however, and may also predict mortality. In this hypothesis-generating review, we summarise available data on the role of endothelial permeability in IPF and focus on the deleterious consequences of sustained endothelial hyperpermeability in response to and during pulmonary inflammation and fibrosis. We propose that persistent permeability and vascular leak in the lung have the potential to establish and amplify the pro-fibrotic environment. Therapeutic interventions aimed at recognising and "plugging" the leak may therefore be of significant benefit for preventing the transition from lung injury to fibrosis and should be areas for future research.

Indexed as

Capillary PermeabilityIdiopathic Pulmonary FibrosisFibrosisHumansLung

Identifiers

PMID32265308
PMCPMC9977144
OpenAlexW3014603300

What OpenQuestion holds

Textmetadata
LicenceTDM
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.