Evidence map›Paper›PMID 21835155›Full record

ArticleThe American journal of pathology2011

Paigen diet-fed apolipoprotein E knockout mice develop severe pulmonary hypertension in an interleukin-1-dependent manner.

Allan Lawrie, Abdul G Hameed, Janet Chamberlain, Nadine Arnold, Aneurin Kennerley, Kay Hopkinson, Josephine Pickworth, David G Kiely, David C Crossman, Sheila E Francis

Open access · hybridAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

48 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
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  4. Article
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  7. Review
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  9. Review
  10. Role of Gut Microbiota in Pulmonary Arterial Hypertension.Frontiers in cellular and infection microbiology · 2022
    Review
  11. Review
  12. Frataxin and endothelial cell senescence in pulmonary hypertension.The Journal of clinical investigation · 2021
    Article
  13. Review
  14. Observational
  15. Article
  16. Cytokines, Chemokines, and Inflammation in Pulmonary Arterial Hypertension.Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. Article
  19. Article
  20. Review
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

10 authors at 3 institutions in 1 country.

Allan LawrieDepartment of Cardiovascular Science, University of Sheffield, Sheffield, United Kingdom. a.lawrie@sheffield.ac.uk
Abdul G Hameed
Janet Chamberlain
Nadine Arnold
Aneurin Kennerley
Kay Hopkinson
Josephine Pickworth
David G Kiely
David C Crossman
Sheila E Francis
University of Sheffield · GBNational Institute for Health Research · GBRoyal Hallamshire Hospital · GB

Funding

Medical Research Council G0800318
6 · The paper itself

Abstract

Inflammatory mechanisms are proposed to play a significant role in the pathogenesis of pulmonary arterial hypertension (PAH). Previous studies have described PAH in fat-fed apolipoprotein E knockout (ApoE(-/-)) mice. We have reported that signaling in interleukin-1-receptor-knockout (IL-1R1(-/-)) mice leads to a reduction in diet-induced systemic atherosclerosis. We subsequently hypothesized that double-null (ApoE(-/-)/IL-1R1(-/-)) mice would show a reduced PAH phenotype compared with that of ApoE(-/-) mice. Male IL-1R1(-/-), ApoE(-/-), and ApoE(-/-)/IL-1R1(-/-) mice were fed regular chow or a high-fat diet (Paigen diet) for 8 weeks before phenotyping for PAH. No abnormal phenotype was observed in the IL-1R1(-/-) mice. Fat-fed ApoE(-/-) mice developed significantly increased right ventricular systolic pressure and substantial pulmonary vascular remodeling. Surprisingly, ApoE(-/-)/IL-1R1(-/-) mice showed an even more severe PAH phenotype. Further molecular investigation revealed the expression of a putative, alternatively primed IL-1R1 transcript expressed within the lungs but not aorta of ApoE(-/-)/IL-1R1(-/-) mice. Treatment of ApoE(-/-) and ApoE(-/-)/IL-1R1(-/-) mice with IL-1-receptor antagonist prevented progression of the PAH phenotype in both strains. Blocking IL-1 signaling may have beneficial effects in treating PAH, and alternative IL-1-receptor signaling in the lung may be important in driving PAH pathogenesis.

Indexed as

AnimalsApolipoproteins EBiomarkersDiet, High-FatDisease ProgressionFeeding BehaviorHemodynamicsHypertension, PulmonaryHypertrophy, Right VentricularInflammation MediatorsInterleukin-1Interleukin 1 Receptor Antagonist ProteinLungMaleMiceMice, Inbred C57BLApolipoproteins EBiomarkersInflammation MediatorsInterleukin-1Interleukin 1 Receptor Antagonist ProteinOsteoprotegerinReceptors, Interleukin-1TNF-Related Apoptosis-Inducing Ligand

Identifiers

PMID21835155
PMCPMC3181351
OpenAlexW2152323727

What OpenQuestion holds

Textmetadata
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.