Evidence map›Paper›PMID 28164246›Full record

ReviewCell and tissue research2017

Immune-mediated inflammation in the pathogenesis of emphysema: insights from mouse models.

John M Craig, Alan L Scott, Wayne Mitzner

Abstract readReview
In one paragraph

Review in Cell and tissue research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Rodent Models of Lung Disease: A Road Map for Translational Research.International journal of molecular sciences · 2025
    Review
  2. Article
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  7. Review
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  10. Antioxidants (Basel, Switzerland) · 2022
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Nasally AdministeredAntioxidants (Basel, Switzerland) · 2020
    Article
  16. Review
  17. Article
  18. Article
  19. 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 1 institution in 1 country.

John M CraigDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, 615 North Wolfe St., Baltimore, MD, USA.
Alan L ScottW. Harry Feinstone Department of Molecular Microbiology and Immunology, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, USA.
Wayne MitznerDepartment of Environmental Health and Engineering, Bloomberg School of Public Health, Johns Hopkins University, 615 North Wolfe St., Baltimore, MD, USA. wmitzner@jhu.edu.
Johns Hopkins University · US

Funding

THE INTEGRATED FUNCTION OF RESPIRATION &CIRCULATIONP01HL010342 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MITZNER, WAYNE · 1985 to 2015
$24.4M
Targeting AP-1 proteins in COPDR03HL096933 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI MITZNER, WAYNE · 2009 to 2010
$164k
Role of the IL-33/ST2 Axis in the Development of EmphysemaF32HL124823 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CRAIG, JOHN MATTHEW · 2014 to 2015
$106k
NHLBI NIH HHS F32 HL124823NHLBI NIH HHS P01 HL010342NHLBI NIH HHS R03 HL096933
6 · The paper itself

Abstract

The cellular mechanisms that result in the initiation and progression of emphysema are clearly complex. A growing body of human data combined with discoveries from mouse models utilizing cigarette smoke exposure or protease administration have improved our understanding of emphysema development by implicating specific cell types that may be important for the pathophysiology of chronic obstructive pulmonary disease. The most important aspects of emphysematous damage appear to be oxidative or protease stress and sustained macrophage activation and infiltration of other immune cells leading to epithelial damage and cell death. Despite the identification of these associated processes and cell types in many experimental studies, the reasons why cigarette smoke and other pollutants result in unremitting damage instead of injury resolution are still uncertain. We propose an important role for macrophages in the sequence of events that lead and maintain this chronic tissue pathologic process in emphysema. This model involves chronic activation of macrophage subtypes that precludes proper healing of the lung. Further elucidation of the cross-talk between epithelial cells that release damage-associated signals and the cellular immune effectors that respond to these cues is a critical step in the development of novel therapeutics that can restore proper lung structure and function to those afflicted with emphysema.

Indexed as

Disease Models, AnimalImmunityAnimalsInflammationMiceModels, BiologicalPulmonary EmphysemaCigarette smokeCOPDElastaseIL-33Macrophage

Identifiers

PMID28164246
PMCPMC5366983
OpenAlexW2585828688

What OpenQuestion holds

Textmetadata
LicenceTDM
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.