Evidence map›Paper›PMID 30306206›Full record

ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2019

A review of inflammatory mechanism in airway diseases.

Parya Aghasafari, Uduak George, Ramana Pidaparti

Abstract readReview
PubMed Publisher
In one paragraph

Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 4 pooled it
16.3field-weighted citation impact, top 1% 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

156 citing papers in PubMed, 4 syntheses or guidelines pooled it, 277 citations in OpenAlex.

  1. Pooled it
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  10. HHIP's dynamic role in epithelial wound healing reveals a potential mechanism of COPD susceptibility.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  16. Pharmacological and Biological Efficacy of Chitosan-Based Materials.International journal of molecular sciences · 2025
    Review
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96 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

3 authors at 1 institution in 1 country.

Parya AghasafariCollege of Engineering, University of Georgia, Athens, GA, USA.
Uduak GeorgeCollege of Engineering, University of Georgia, Athens, GA, USA.
Ramana PidapartiCollege of Engineering, University of Georgia, Athens, GA, USA. rmparti@uga.edu.
University of Georgia · US

Funding

National Science Foundation 1430379
6 · The paper itself

Abstract

backgroundInflammation in the lung is the body's natural response to injury. It acts to remove harmful stimuli such as pathogens, irritants, and damaged cells and initiate the healing process. Acute and chronic pulmonary inflammation are seen in different respiratory diseases such as; acute respiratory distress syndrome, chronic obstructive pulmonary disease (COPD), asthma, and cystic fibrosis (CF).

findingsIn this review, we found that inflammatory response in COPD is determined by the activation of epithelial cells and macrophages in the respiratory tract. Epithelial cells and macrophages discharge transforming growth factor-β (TGF-β), which trigger fibroblast proliferation and tissue remodeling. Asthma leads to airway hyper-responsiveness, obstruction, mucus hyper-production, and airway-wall remodeling. Cytokines, allergens, chemokines, and infectious agents are the main stimuli that activate signaling pathways in epithelial cells in asthma. Mutation of the CF transmembrane conductance regulator (CFTR) gene results in CF. Mutations in CFTR influence the lung epithelial innate immune function that leads to exaggerated and ineffective airway inflammation that fails to abolish pulmonary pathogens. We present mechanistic computational models (based on ordinary differential equations, partial differential equations and agent-based models) that have been applied in studying the complex physiological and pathological mechanisms of chronic inflammation in different airway diseases.

conclusionThe scope of the present review is to explore the inflammatory mechanism in airway diseases and highlight the influence of aging on airways' inflammation mechanism. The main goal of this review is to encourage research collaborations between experimentalist and modelers to promote our understanding of the physiological and pathological mechanisms that control inflammation in different airway diseases.

Indexed as

AgingAnimalsHumansInflammationLungModels, BiologicalRespiratory Tract DiseasesAirway diseaseComputational modelingInflammagingInflammation

Identifiers

PMID30306206
OpenAlexW2895841640

What OpenQuestion holds

Textmetadata
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.