Evidence map›Paper›PMID 26637347›Full record

ArticleMolecular and cellular pediatrics2015

Airway reactivity and sphingolipids-implications for childhood asthma.

Jennie G Ono, Tilla S Worgall, Stefan Worgall

Open access · goldAbstract read
In one paragraph

Article in Molecular and cellular pediatrics, 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
2.3field-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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Metabolomic profiling of lung function in Costa-Rican children with asthma.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Trial
  2. Plasma metabolomics in infancy reveals early signatures of a stringently-defined otitis-prone phenotype.Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology · 2026
    Article
  3. Review
  4. Review
  5. Linking Lipid Metabolism and Immune Function: New Insights into Chronic Respiratory Diseases.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Orosomucoid-like protein 3, rhinovirus and asthma.World journal of critical care medicine · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Orosomucoid-like 3 Supports Rhinovirus Replication in Human Epithelial Cells.American journal of respiratory cell and molecular biology · 2020
    Article
  17. Article
  18. Article
  19. Pathway analysis of a genome-wide gene by air pollution interaction study in asthmatic children.Journal of exposure science & environmental epidemiology · 2019
    Article
  20. Crucial Role of Extracellular Vesicles in Bronchial Asthma.International journal of molecular sciences · 2019
    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

3 authors at 2 institutions in 1 country.

Jennie G OnoDepartment of Pediatrics, Weill Cornell Medical College, 505 East 70th Street, Box 211, New York, NY, 10021, USA.
Tilla S WorgallDepartment of Pathology, Columbia University, New York, NY, USA.
Stefan WorgallDepartment of Pediatrics, Weill Cornell Medical College, 505 East 70th Street, Box 211, New York, NY, 10021, USA. stw2006@med.cornell.edu.
Cornell University · USColumbia University · US

Funding

Clinical and Translational Science CenterUL1TR000457 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$46.0M
Clinical and Translational Science CenterKL2TR000458 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI IMPERATO-MCGINLEY, JULIANNE L · 2012 to 2016
$2.1M
NCATS NIH HHS KL2 TR000458NCATS NIH HHS UL1 TR000457
6 · The paper itself

Abstract

Asthma is a clinically heterogeneous disorder, whose onset and progression results from a complex interplay between genetic susceptibility, allergens, and viral triggers. Sphingolipids and altered sphingolipid metabolism have emerged as potential key contributors to the pathogenesis of asthma. Orosomucoid-like 3 gene (ORMDL3) and the asthma susceptibility locus 17q21 have been strongly and reproducibly linked to childhood asthma, but how this gene is functionally linked to asthma is incompletely understood. ORMDL proteins play an integral role in sphingolipid homeostasis and synthesis, and asthma-associated ORMDL3 polymorphisms have been associated with early viral respiratory infections and increased risk of asthma. ORMDL proteins act as inhibitors of serine palmitoyl-CoA transferase (SPT), the rate-limiting enzyme for de novo sphingolipid synthesis, and decreased sphingolipid synthesis through SPT increases airway hyperreactivity, which is independent of allergy or inflammation. In allergic models of asthma, the sphingolipid mediators sphingosine-1-phosphate (S1P) and ceramide have been shown to be important signaling molecules for airway hyperreactivity, mast cell activation, and inflammation. This review will highlight how sphingolipids and altered sphingolipid metabolism may contribute towards the underlying mechanisms of childhood asthma.

Indexed as

Airway hyperreactivityAsthmaORMDL3RhinovirusSphingolipidsSPT

Identifiers

PMID26637347
PMCPMC4670439
OpenAlexW2183920120

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.