Evidence map›Paper›PMID 24982697›Full record

ReviewThe World Allergy Organization journal2014

Systems biology approaches to understanding Epithelial Mesenchymal Transition (EMT) in mucosal remodeling and signaling in asthma.

Talha Ijaz, Konrad Pazdrak, Mridul Kalita, Rolf Konig, Sanjeev Choudhary, Bing Tian, Istvan Boldogh, Allan R Brasier

Open access · goldAbstract readReview
In one paragraph

Review in The World Allergy Organization journal, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

74 citing papers in PubMed, 124 citations in OpenAlex.

  1. Article
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  15. Article
  16. Subsets of Eosinophils in Asthma, a Challenge for Precise Treatment.International journal of molecular sciences · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Review

14 more citing papers are in PubMed but not listed here.

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

8 authors at 1 institution in 1 country.

Talha Ijaz *Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Konrad Pazdrak *Department of Biochemistry and Molecular Biology, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Mridul Kalita *Sealy Center for Molecular Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Rolf KonigSealy Center for Molecular Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Sanjeev ChoudharyDepartment of Biochemistry and Molecular Biology, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Bing TianDepartment of Internal Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Istvan BoldoghDepartment of Biochemistry and Molecular Biology, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
Allan R BrasierSealy Center for Molecular Medicine, The University of Texas Medical Branch, 301 University Blvd, Galveston 77555-1060, Texas, USA.
The University of Texas Medical Branch at Galveston · US

Funding

Virus, Tissue Culture and ImmunoassayP01AI062885 · NIAID · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI GAROFALO, ROBERTO P · 2005 to 2022
$23.9M
Synthetic Organic Chemistry CoreP30ES006676 · NIEHS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI ELFERINK, CORNELIS JOHAN · 1995 to 2017
$21.7M
NIAID NIH HHS P01 AI062885NIEHS NIH HHS P30 ES006676
6 · The paper itself

Abstract

A pathological hallmark of asthma is chronic injury and repair, producing dysfunction of the epithelial barrier function. In this setting, increased oxidative stress, growth factor- and cytokine stimulation, together with extracellular matrix contact produces transcriptional reprogramming of the epithelial cell. This process results in epithelial-mesenchymal transition (EMT), a cellular state associated with loss of epithelial polarity, expression of mesenchymal markers, enhanced mobility and extracellular matrix remodeling. As a result, the cellular biology of the EMT state produces characteristic changes seen in severe, refractory asthma: myofibroblast expansion, epithelial trans-differentiation and subepithelial fibrosis. EMT also induces profound changes in epithelial responsiveness that affects innate immune signaling that may have impact on the adaptive immune response and effectiveness of glucocorticoid therapy in severe asthma. We discuss how this complex phenotype is beginning to be understood using systems biology-level approaches through perturbations coupled with high throughput profiling and computational modeling. Understanding the distinct changes induced by EMT at the systems level may provide translational strategies to reverse the altered signaling and physiology of refractory asthma.

Indexed as

EMTEosinophilsInflammationInnate immunityNF-κBSystems biologyTGFβ

Identifiers

PMID24982697
PMCPMC4068075
OpenAlexW2139935404

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.