Evidence map›Paper›PMID 25553258›Full record

ReviewAllergy, asthma & immunology research2015

Chitotriosidase in the Pathogenesis of Inflammation, Interstitial Lung Diseases and COPD.

Soo Jung Cho, Michael D Weiden, Chun Geun Lee

Open access · hybridAbstract readReview
In one paragraph

Review in Allergy, asthma & immunology research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
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  5. Article
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  7. Article
  8. Phenotypes and Serum Biomarkers in Sarcoidosis.Diagnostics (Basel, Switzerland) · 2024
    Review
  9. Particulate matterRespiratory research · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Tobacco Smoke Exposure Exacerbated Crystalline Silica-Induced Lung Toxicity in Rats.Toxicological sciences : an official journal of the Society of Toxicology · 2020
    Article
  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

3 authors at 3 institutions in 1 country.

Soo Jung ChoDivision of Pulmonary and Critical Care Medicine, New York-Presbyterian Hospital-Weill Cornell Medical Center, Weill Cornell Medical College, New York, NY, USA.
Michael D WeidenDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, New York University School of Medicine, New York, NY, USA. ; New York University, School of Medicine, Department of Environmental Medicine, Tuxedo Park, NY, USA. ; Bureau of Health Services and Office of Medical Affairs Fire Department of New York, Brooklyn, NY, USA.
Chun Geun LeeMolecular Microbiology and Immunology, Brown University,Warren Alpert School of Medicine Box G-L, Providence, RI, USA.
Brown University · USCornell University · USNew York University · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
Chitinase1 as a Biomarker and Therapeutic Target in Scleroderma Lung DiseaseR01HL115813 · NHLBI · BROWN UNIVERSITY · PI LEE, CHUN GEUN · 2014 to 2017
$1.5M
NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL115813
6 · The paper itself

Abstract

As a member of 18 glycosyl hydrolase (GH) family, chitotriosidase (Chitinase 1, CHIT1) is a true chitinase mainly expressed in the differentiated and polarized macrophages. CHIT1 is an innate immune mediator that digests the cell walls of chitin-containing eukaryotic pathogens, such as fungi. However, CHIT1 is dysregulated in granulomatous and fibrotic interstitial lung diseases characterized by inflammation and tissue remodeling. These include tuberclosis, sarcoidosis, idiopathic pulmonary fibrosis, scleroderma-associated interstitial lung diseases (SSc-ILD), and chronic obstructive lung diseases (COPD). CHIT1 serum concentration correlates with the progression or the severity of these diseases, suggesting a potential use of CHIT1 as a biomarker or a therapeutic target. Recent studies with genetically modified mice demonstrate that CHIT1 enhances TGF-β1 receptor expression and signaling, suggesting a role in initiating or amplifying the response to organ injury and repair. This additional CHIT1 activity is independent of its enzymatic activity. These studies suggest that CHIT1 serves a bridging function; it is both an innate immune mediator and a regulator of tissue remodeling. This review will focus on recent data linking CHIT1 to the pathogenesis of inflammation, interstitial lung disease, and COPD.

Indexed as

Chitotriosidaseidiopathic pulmonary fibrosisinflammationsarcoidosissclerodermaTGF-beta

Identifiers

PMID25553258
PMCPMC4274464
OpenAlexW2162870516

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.