Evidence map›Paper›PMID 28992358›Full record

ArticleImmunology2018

Role of Galectin-3 in the pathophysiology underlying allergic lung inflammation in a tissue inhibitor of metalloproteinases 1 knockout model of murine asthma.

Manoj J Mammen, Mark F Sands, Elaine Abou-Jaoude, Ravikumar Aalinkeel, Jessica L Reynolds, Neil U Parikh, Umesh Sharma, Stanley A Schwartz, Supriya D Mahajan

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

7 citing papers in PubMed, 12 citations in OpenAlex.

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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

9 authors at 2 institutions in 1 country.

Manoj J MammenDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Mark F SandsDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Elaine Abou-JaoudeDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Ravikumar AalinkeelDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Jessica L ReynoldsDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Neil U ParikhDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Umesh SharmaDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Stanley A SchwartzDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.
Supriya D MahajanDepartment of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA.ORCID 0000-0002-5298-6962
University at Buffalo, State University of New York · USVA Western New York Healthcare System · US

Funding

University of Buffalo Clinical and Translational Science Institute - Supplement SchulyerUL1TR001412 · NCATS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MURPHY, TIMOTHY F · 2015 to 2024
$33.8M
Galectin-3-Mediated Post-Ischemic Myocardial Dysfunction and its Inhibition by a Novel Peptide N-Acetyl-Seryl-Aspartyl-Lysyl-ProlineK08HL131987 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SHARMA, UMESH C · 2017 to 2021
$987k
NCATS NIH HHS UL1 TR001412NHLBI NIH HHS K08 HL131987
6 · The paper itself

Abstract

Asthma is a chronic inflammatory respiratory disease characterized by airway inflammation, airway hyperresponsiveness and reversible airway obstruction. Understanding the mechanisms that underlie the various endotypes of asthma could lead to novel and more personalized therapies for individuals with asthma. Using a tissue inhibitor of metalloproteinases 1 (TIMP-1) knockout murine allergic asthma model, we previously showed that TIMP-1 deficiency results in an asthma phenotype, exhibiting airway hyperreactivity, enhanced eosinophilic inflammation and T helper type 2 cytokine gene and protein expression following sensitization with ovalbumin. In the current study, we compared the expression of Galectins and other key cytokines in a murine allergic asthma model using wild-type and TIMP-1 knockout mice. We also examined the effects of Galectin-3 (Gal-3) inhibition on a non-T helper type 2 cytokine interleukin-17 (IL-17) to evaluate the relationship between Gal-3 and the IL-17 axis in allergic asthma. Our results showed a significant increase in Gal-3, IL-17 and transforming growth factor-β

Indexed as

A549 CellsAnimalsAsthmaBronchial HyperreactivityCell Line, TumorCytokinesDisease Models, AnimalGalectin 3HumansLungMiceMice, KnockoutPneumoniaRespiratory HypersensitivityTh2 CellsTissue Inhibitor of Metalloproteinase-1CytokinesGalectin 3Timp1 protein, mouseTissue Inhibitor of Metalloproteinase-1AsthmaGalectin-3IL-17tissue inhibitor of metalloproteinases 1

Identifiers

PMID28992358
PMCPMC5795177
OpenAlexW2763004693

What OpenQuestion holds

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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.