Evidence map›Paper›PMID 42298125›Full record

ArticleCommunications biology2026

KLF6 activation marks an angiogenic and apoptosis resistant endothelial phenotype in pulmonary arterial hypertension.

Rehab Alharbi, Merve Keles, Nadia Fernandes, Hannah Maude, Adam Fellows, Richard D Williams, Chien-Nien Chen, Nathalie Lambie, Nik Matthews, May Al-Sahaf and 7 more

Abstract read
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In one paragraph

Article in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Rehab AlharbiNational Heart and Lung Institute, Imperial College London, London, UK.
Merve KelesNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0002-5212-3753
Nadia FernandesSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.ORCID 0000-0003-4595-9939
Hannah MaudeSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.
Adam FellowsNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0002-9975-3795
Richard D WilliamsSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.
Chien-Nien ChenNational Heart and Lung Institute, Imperial College London, London, UK.
Nathalie LambieSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.ORCID 0009-0005-0440-5894
Nik MatthewsSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.ORCID 0000-0002-0602-1131
May Al-SahafNational Heart and Lung Institute, Imperial College London, London, UK.
Sam N BarnettNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0002-8968-4319
Minzhe GuoThe Perinatal Institute and Section of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID 0000-0002-5502-9172
Lan ZhaoNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0003-1177-5568
Allan LawrieNational Heart and Lung Institute, Imperial College London, London, UK.ORCID 0000-0003-4192-9505
Jeffrey A WhitsettThe Perinatal Institute and Section of Neonatology, Perinatal and Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.ORCID 0000-0003-1668-5174
Inês CebolaSection of Genetics and Genomics, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.ORCID 0000-0003-3528-4982
Beata Wojciak-StothardNational Heart and Lung Institute, Imperial College London, London, UK. b.wojciak-stothard@imperial.ac.uk.ORCID 0000-0002-6607-7372

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary arterial hypertension (PAH) is a severe, currently incurable lung disease characterized by endothelial injury and excessive repair, leading to arterial narrowing. However, the contributory mechanisms remain poorly understood. Here we show that Krüppel-like factor 6 (KLF6) is a feature of vascular pathology in PAH. KLF6 expression is elevated in human PAH and preclinical models of PAH and promotes endothelial repair and angiogenesis through transcriptomic remodelling, with effects distinct from those of KLF2 and KLF4. Endothelial KLF6 also stimulates vascular smooth muscle cell proliferation, which is attenuated by bosentan and imatinib. DisGeNET and spatial transcriptomic analyses of control and PAH lungs reveal elevated KLF6 in PAH endothelium, endothelial progenitor cells, and PAH with alveolar capillary dysplasia. In summary, KLF6 activation uniquely orchestrates endothelial repair and is a feature of the angio-proliferative vascular phenotype in PAH.

Indexed as

AngiogenesisApoptosisEndothelial CellsEndothelium, VascularKruppel-Like Factor 6Neovascularization, PathologicPulmonary Arterial HypertensionAnimalsCell ProliferationHumansMaleMicePhenotypeKLF6 protein, humanKruppel-Like Factor 6

Identifiers

PMID42298125
PMCPMC13282386

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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.