Evidence map›Paper›PMID 25984393›Full record

ArticleJournal of allergy & therapy2012

S100A12 and the Airway Smooth Muscle: Beyond Inflammation and Constriction.

Blanca Camoretti-Mercado, Eltayeb Karrar, Luis Nuñez, Marion A Hofmann Bowman

Open access · hybridAbstract read
In one paragraph

Article in Journal of allergy & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.4field-weighted citation impact, top 36% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Inflammatory bowel disease biomarkers.Medicinal research reviews · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. 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

4 authors at 1 institution in 1 country.

Blanca Camoretti-MercadoDepartment of Medicine, Section of Pulmonary and Critical Care, University of Chicago, USA.
Eltayeb KarrarDepartment of Medicine, Section of Pulmonary and Critical Care, University of Chicago, USA.
Luis NuñezDepartment of Medicine, Section of Pulmonary and Critical Care, University of Chicago, USA ; BioTarget, USA.
Marion A Hofmann BowmanDepartment of Medicine,Section of Cardiology, University of Chicago, USA.
University of Chicago · US

Funding

TRANSLATIONAL RESEARCH UNIVERSITY OF CHICAGO: CLINICAL TRIALSUL1RR024999 · NCRR · UNIVERSITY OF CHICAGO · PI SOLWAY, JULIAN · 2007 to 2011
$25.3M
Pro-inflammatory S100 protein as disease modifier in calcific aortic valve diseasR01HL114821 · NHLBI · UNIVERSITY OF CHICAGO · PI HOFMANN BOWMAN, MARION A · 2012 to 2015
$1.5M
Role of TGF beta in Airway Hyperresponsiveness in VivoK01HL092588 · NHLBI · UNIVERSITY OF SOUTH FLORIDA · PI CAMORETTI-MERCADO, BLANCA · 2008 to 2012
$649k
Pro-inflammatory S100A12 in atherosclerosis and acute coronary syndromeK08HL090917 · NHLBI · UNIVERSITY OF CHICAGO · PI HOFMANN BOWMAN, MARION A · 2008 to 2012
$621k
NCRR NIH HHS UL1 RR024999NHLBI NIH HHS K01 HL092588NHLBI NIH HHS K08 HL090917NHLBI NIH HHS R01 HL114821
6 · The paper itself

Abstract

Airway inflammation, lung remodeling, and Airway Hyperresponsiveness (AHR) are major features of asthma and Chronic Obstructive Pulmonary Disease (COPD). The inflammatory response to allergens, air pollutants, and other insults is likely to play a key role in promoting structural changes in the lung including the overabundance of Airway Smooth Muscle (ASM) seen in asthmatics. These alterations or remodeling could, in turn, impact the immunmodulatory actions of the ASM, the ASM's contractile properties, and the development of AHR. New evidences suggest that airway inflammation and AHR are not tightly related to each other and that the structural component of the airway, mainly the ASM, is a chief driver of AHR. Members of the S100/calgranulins family have been implicated in the regulation of inflammation and cell apoptosis in various systems. S100A12 is highly expressed in neutrophils and is one of the most abundant proteins in the lungs of patients with asthma or COPD. Studies with genetic engineered mice with smooth muscle cell-targeted expression of human S100A12 revealed that S100A12 reduces airway smooth muscle amounts and dampens airway inflammation and airway hyperreactivity in a model of allergic lung inflammation. Thus, targeting airway smooth muscle for instance through delivery of pro-apoptotic S100A12 could represent an attractive means to promote ASM apoptosis and to reduce ASM abundance in asthmatics.

Identifiers

PMID25984393
PMCPMC4431649
OpenAlexW2332431593

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.