Evidence map›Paper›PMID 40590703›Full record

ArticleDisease models & mechanisms2025

An in vitro model of the epithelial airway reveals a key function for EHF in lung homeostasis and disease.

Laetitia Pinte, Marta Vila-Gonzalez, Eleanor C Williams, Erika Causa, Ricardo Fradique, Tekle Pauzaite, Charlotte Passemar, Silvia Becca, Christopher Gribben, Shiqi Ye and 8 more

Abstract read
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Article in Disease models & mechanisms, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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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.

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2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

18 authors.

Laetitia PinteWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.ORCID 0009-0002-2732-8949
Marta Vila-GonzalezWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Eleanor C WilliamsWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Erika CausaCavendish Laboratory, University of Cambridge, Cambridge CB3 0HE, UK.
Ricardo FradiqueCavendish Laboratory, University of Cambridge, Cambridge CB3 0HE, UK.
Tekle PauzaiteCambridge Institute of Therapeutic and Infectious Disease, University of Cambridge, Cambridge CB2 0AW, UK.
Charlotte PassemarMRC Laboratory of Molecular Biology, University of Cambridge, Cambridge CB2 0AW, UK.
Silvia BeccaWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Christopher GribbenWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Shiqi YeWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Maha Al-ThaniDepartment of Surgery, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Cambridge CB2 0AW, UK.
Fabian BachingerWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Floris J M RoosWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
James A NathanWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Irina MohorianuWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.
Andres FlotoStroke Research Group, Department of Clinical Neurosciences, University of Cambridge, Cambridge CB2 0QQ, UK.
Pietro CicutaCavendish Laboratory, University of Cambridge, Cambridge CB3 0HE, UK.
Ludovic VallierWellcome - MRC Cambridge Stem Cell Institute, University of Cambridge, Cambridge CB2 0AW, UK.

Funding

Cystic Fibrosis Trust IH001Cystic Fibrosis Trust SRC 016European Research Council ERC741707European UnionUniversity of CambridgeWellcome - MRC Cambridge Stem Cell InstituteWellcome TrustWellcome Trust 203151/Z/16/Z
6 · The paper itself

Abstract

In the lung airways, multiple cell types facilitate airflow to alveoli, clearing out debris, particles and pathogens. These vital processes are impeded in chronic inflammatory respiratory diseases, in which the epithelium typically suffers from inflammation, infections and hypoxia. An increasing body of evidence highlights the critical role of modifier genes in responses and resistance against these pathogenic processes. Here, we sought to study the transcription factor EHF, suggested by previous studies as a putative modifier gene, yet its functional role remains ambiguous. To explore this question, we knocked out EHF in human induced pluripotent stem cell-derived lung cells and examined the subsequent phenotypic and functional impacts. Loss of EHF enhanced cystic fibrosis transmembrane conductance regulator activity, led to transcriptomic changes in basal cells, increased transepithelial electrical resistance and reduced HIF-1α-mediated response to hypoxia. Here, we show that variation in EHF expression can impact lung diseases through several mechanisms, thereby highlighting prospects for novel therapies.

Indexed as

Epithelial CellsHomeostasisLungLung DiseasesModels, BiologicalTranscription FactorsCell HypoxiaCystic Fibrosis Transmembrane Conductance RegulatorElectric ImpedanceGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitInduced Pluripotent Stem CellsPhenotypeTranscriptomeCystic Fibrosis Transmembrane Conductance RegulatorHypoxia-Inducible Factor 1, alpha SubunitTranscription FactorsDisease modellingInduced pluripotent stem cellsLung airway pathophysiologyStem cell biology

Identifiers

PMID40590703
PMCPMC12264733

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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.