ArticleProceedings of the National Academy of Sciences of the United States of America2026
Interleukin-6 is critical in the development of pulmonary vascular disease in
Max Schwiening, Qingyue Gao, Mark Southwood, Alexi Crosby, Stephen Moore, Jose A Valer, Niki Veale, Benjamin J Dunmore, Paul D Upton, A A Roger Thompson and 3 more
Abstract read
In one paragraphArticle in Proceedings of the National Academy of Sciences of the United States of America, 2026. 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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0cells of the map it votes in
0citing papers in PubMed
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1 · What the graph read from itWhat 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 registryThe trial behind it
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3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
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4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
13 authors.
Max SchwieningCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.
Qingyue GaoCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.
Mark SouthwoodDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Alexi CrosbyDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Stephen MooreDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Jose A ValerCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0003-1184-9491 Niki VealeCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0009-0000-4023-7553 Benjamin J DunmoreCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.
Paul D UptonDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
A A Roger ThompsonDivision of Clinical Medicine, University of Sheffield, Sheffield S10 2RX, United Kingdom.ORCID 0000-0002-0717-4551 Nicholas W MorrellDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
Stefan J MarciniakCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0001-8472-7183 Elaine SoonCambridge Institute for Medical Research, University of Cambridge, Cambridge CB2 0XY, United Kingdom.ORCID 0000-0002-5744-5014 Funding
Medical Research Council MR/R008051/1Wellcome Trust
6 · The paper itselfAbstract
Biallelic mutations in EIF2AK4, encoding Eukaryotic Translation Initiation Factor 2α kinase 4 or General Control Nonderepressible 2 (GCN2), cause pulmonary veno-occlusive disease (PVOD), a fatal form of pulmonary hypertension. The mechanisms linking GCN2 deficiency with pulmonary vascular pathology are poorly understood. To investigate this, we developed two mouse models: genetic ablation of
Indexed as
Hypertension, PulmonaryInterleukin-6Protein Serine-Threonine KinasesPulmonary Veno-Occlusive DiseaseAnimalsDisease Models, AnimalFibroblastsLungMiceMice, Inbred C57BLMice, KnockoutMitomycinSignal TransductionEif2ak4 protein, mouseInterleukin-6interleukin-6, mouseMitomycinProtein Serine-Threonine KinasesGCN2interleukin-6pulmonary veno-occlusive disease
Identifiers
PMID42406961
PMCPMC13367861
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