Evidence map›Paper›PMID 26355153›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

Fstl1 Promotes Asthmatic Airway Remodeling by Inducing Oncostatin M.

Marina Miller, Andrew Beppu, Peter Rosenthal, Alexa Pham, Sudipta Das, Maya Karta, Dae Jin Song, Christine Vuong, Taylor Doherty, Michael Croft and 7 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 49 citations in OpenAlex.

  1. MrgprC11American journal of respiratory cell and molecular biology · 2025
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Observational
  10. FSTL1 aggravates OVA-induced inflammatory responses by activating the NLRP3/IL-1β signaling pathway in mice and macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  11. Article
  12. Mechanisms forFrontiers in allergy · 2021
    Article
  13. Article
  14. Article
  15. FSTL-1: A New Player in the Prevention of Emphysema.American journal of respiratory and critical care medicine · 2020
    Article
  16. FSTL-1 Attenuation Causes Spontaneous Smoke-Resistant Pulmonary Emphysema.American journal of respiratory and critical care medicine · 2020
    Article
  17. Review
  18. Review
  19. Follistatin-like 1 in development and human diseases.Cellular and molecular life sciences : CMLS · 2018
    Review
  20. Article
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 at 6 institutions in 6 countries.

Marina MillerDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Andrew BeppuDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Peter RosenthalDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Alexa PhamDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Sudipta DasDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Maya KartaDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Dae Jin SongDepartment of Pediatrics, Korea University College of Medicine, Seoul 02841, Korea;
Christine VuongDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Taylor DohertyDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Michael CroftDivision of Immune Regulation, La Jolla Institute for Allergy and Immunology, La Jolla, CA 92037;
Bruce ZurawDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093;
Xu ZhangInstitute of Neuroscience, Shanghai Institute for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;
Xiang GaoModel Animal Research Center, Nanjing University, Nanjing 210061, China;
Seema AcevesDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093; Department of Pediatrics, University of California, San Diego, La Jolla, CA 92093; and.
Fazila ChouialiMeakins-Christie Laboratories of McGill University and McGill University Health Center Research Institute, Montreal, Quebec H2X 2p2, Canada.
Qutayba HamidMeakins-Christie Laboratories of McGill University and McGill University Health Center Research Institute, Montreal, Quebec H2X 2p2, Canada.
David H BroideDepartment of Medicine, University of California, San Diego, La Jolla, CA 92093; dbroide@ucsd.edu.
University of California, San Diego · USMcGill University · CAChinese Academy of Sciences · CNKorea University · KRLa Jolla Institute for Immunology · USNanjing University · CN

Funding

TRM and airway inflammation and remodelingU19AI070535 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2006 to 2025
$34.2M
TRAINING IN MOLECULAR &CELL BIOLOGY OF ALLERGYT32AI007469 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 1994 to 2024
$6.9M
Chromosome 17q, allergic inflammation, and remodelingR01AI107779 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2013 to 2024
$4.7M
Eosinophil trafficking and chronic tissue damage induced by allergic inflammationR37AI038425 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2007 to 2016
$3.7M
RBM3 regulation of type 2 innate lymphoid cells in allergic inflammationR01AI114585 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DOHERTY, TAYLOR A · 2015 to 2019
$2.3M
Eosinophil TraffickingR01AI038425 · NIAID · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI BROIDE, DAVID H · 1996 to 2005
$1.8M
Siglec-F and Resolution of Allergic InflammationR01AI072115 · NIAID · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BROIDE, DAVID H · 2008 to 2012
$1.7M
NIAID NIH HHS AI 107779NIAID NIH HHS AI 38425NIAID NIH HHS AI 70535NIAID NIH HHS AI 72115NIAID NIH HHS R01 AI038425NIAID NIH HHS R01 AI072115NIAID NIH HHS R01 AI107779NIAID NIH HHS R01 AI114585NIAID NIH HHS R37 AI038425NIAID NIH HHS T32 AI007469NIAID NIH HHS U19 AI070535
6 · The paper itself

Abstract

Chronic asthma is associated with airway remodeling and decline in lung function. In this article, we show that follistatin-like 1 (Fstl1), a mediator not previously associated with asthma, is highly expressed by macrophages in the lungs of humans with severe asthma. Chronic allergen-challenged Lys-Cre(tg) /Fstl1(Δ/Δ) mice in whom Fstl1 is inactivated in macrophages/myeloid cells had significantly reduced airway remodeling and reduced levels of oncostatin M (OSM), a cytokine previously not known to be regulated by Fstl1. The importance of the Fstl1 induction of OSM to airway remodeling was demonstrated in murine studies in which administration of Fstl1 induced airway remodeling and increased OSM, whereas administration of an anti-OSM Ab blocked the effect of Fstl1 on inducing airway remodeling, eosinophilic airway inflammation, and airway hyperresponsiveness, all cardinal features of asthma. Overall, these studies demonstrate that the Fstl1/OSM pathway may be a novel pathway to inhibit airway remodeling in severe human asthma.

Indexed as

Airway RemodelingAnimalsAntibodiesAsthmaFemaleFollistatin-Related ProteinsHumansMacrophagesMaleMiceOncostatin MSignal TransductionAntibodiesFollistatin-Related ProteinsFSTL1 protein, humanFstl1 protein, mouseOncostatin M

Identifiers

PMID26355153
PMCPMC4811198
OpenAlexW1856330428

What OpenQuestion holds

Textmetadata
LicenceTDM
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.