Evidence map›Paper›PMID 24160323›Full record

ArticleThe American journal of pathology2013

Treatment with anti-gremlin 1 antibody ameliorates chronic hypoxia/SU5416-induced pulmonary arterial hypertension in mice.

Loredana Ciuclan, Kellyann Sheppard, Liqun Dong, Daniel Sutton, Nicholas Duggan, Martin Hussey, Jenny Simmons, Nicholas W Morrell, Gabor Jarai, Matthew Edwards and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

44 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Article
  8. Article
  9. GREM1 signaling in cancer: tumor promotor and suppressor?Journal of cell communication and signaling · 2023
    Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Gremlin: a complex molecule regulating wound healing and fibrosis.Cellular and molecular life sciences : CMLS · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. Article
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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

14 authors at 4 institutions in 2 countries.

Loredana CiuclanRespiratory Disease Area, Novartis Institutes for BioMedical Research, Horsham, West Sussex, United Kingdom.
Kellyann Sheppard
Liqun Dong
Daniel Sutton
Nicholas Duggan
Martin Hussey
Jenny Simmons
Nicholas W Morrell
Gabor Jarai
Matthew Edwards
Gerald Dubois
Matthew Thomas
Gino Van Heeke
Karen England
Genomics Institute of the Novartis Research Foundation · USPathways Behavioral Services · USNovartis (United Kingdom) · GBUniversity of Cambridge · GB

Funding

TISSUE DISTRIBUTION FOR RARE DISEASE RESEARCHU42RR006042 · NCRR · NATIONAL DISEASE RESEARCH INTERCHANGE · PI LONSDALE, JOHN T · 1991 to 2011
$16.5M
British Heart Foundation RG/13/4/30107NCRR NIH HHS 5 U42 RR006042NCRR NIH HHS U42 RR006042
6 · The paper itself

Abstract

The expression of the bone morphogenetic protein antagonist, Gremlin 1, was recently shown to be increased in the lungs of pulmonary arterial hypertension patients, and in response to hypoxia. Gremlin 1 released from the vascular endothelium may inhibit endogenous bone morphogenetic protein signaling and contribute to the development of pulmonary arterial hypertension. Here, we investigate the impact of Gremlin 1 inhibition in disease after exposure to chronic hypoxia/SU5416 in mice. We investigated the effects of an anti-Gremlin 1 monoclonal antibody in the chronic hypoxia/SU5416 murine model of pulmonary arterial hypertension. Chronic hypoxic/SU5416 exposure of mice induced upregulation of Gremlin 1 mRNA in lung and right ventricle tissue compared with normoxic controls. Prophylactic treatment with an anti-Gremlin 1 neutralizing mAb reduced the hypoxic/SU5416-dependent increase in pulmonary vascular remodeling and right ventricular hypertrophy. Importantly, therapeutic treatment with an anti-Gremlin 1 antibody also reduced pulmonary vascular remodeling and right ventricular hypertrophy indicating a role for Gremlin 1 in the progression of the disease. We conclude that Gremlin 1 plays a role in the development and progression of pulmonary arterial hypertension in the murine hypoxia/SU5416 model, and that Gremlin 1 is a potential therapeutic target for pulmonary arterial hypertension.

Indexed as

AnimalsAntibodies, MonoclonalBone Morphogenetic ProteinsChronic DiseaseCytokinesFamilial Primary Pulmonary HypertensionHeart VentriclesHEK293 CellsHemodynamicsHumansHypertension, PulmonaryHypoxiaIndolesIntercellular Signaling Peptides and ProteinsLungMiceAntibodies, MonoclonalBone Morphogenetic ProteinsCytokinesGREM1 protein, humanGrem1 protein, mouseIndolesIntercellular Signaling Peptides and ProteinsPyrrolesSemaxinib

Identifiers

PMID24160323
PMCPMC5691347
OpenAlexW1993551856

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.