Evidence map›Paper›PMID 27021937›Full record

ReviewThe American journal of pathology2016

Mechanisms of Lung Fibrosis Resolution.

Stephan W Glasser, James S Hagood, Simon Wong, Carmen A Taype, Satish K Madala, William D Hardie

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
10.2field-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

90 citing papers in PubMed, 142 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026
    Review
  11. Article
  12. Review
  13. Review
  14. Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025
    Review
  15. The Role of Particle Inhalation in Idiopathic Pulmonary Fibrosis.International journal of molecular sciences · 2025
    Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

30 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

6 authors at 2 institutions in 1 country.

Stephan W GlasserDivision of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
James S HagoodDivision of Pediatric Respiratory Medicine, University of California-San Diego, La Jolla, California; Division of Respiratory Medicine, Rady Children's Hospital of San Diego, San Diego, California.
Simon WongDivision of Pediatric Respiratory Medicine, University of California-San Diego, La Jolla, California.
Carmen A TaypeDivision of Pulmonary, Critical Care, and Sleep Medicine, University of California-San Diego, La Jolla, California.
Satish K MadalaDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio.
William D HardieDivision of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio. Electronic address: william.hardie@cchmc.org.
Cincinnati Children's Hospital Medical Center · USUniversity of California, San Diego · US

Funding

Regulation of Fibroblast Phenotype in Lung FibrosisR01HL082818 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2007 to 2017
$3.7M
Biomarkers of Immunologic Function and Preterm Respiratory OutcomesU01HL101800 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI CHOUGNET, CLAIRE A., JOBE, ALAN H · 2010 to 2014
$2.5M
Targeting the Apoptosis-Resistant Pulmonary MyofibroblastR01HL111169 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI HAGOOD, JAMES S. · 2012 to 2015
$1.7M
Hypoxia Signaling and Spontaneous Pulmonary Fibrosis in a Novel Mouse ModelR21AG047473 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI DAVE, VRUSHANK · 2015 to 2016
$426k
THE ROLE OF IL-31 IN TH2 CYTOKINE-DRIVEN SYSTEMIC SCLEROSISR03AR062832 · NIAMS · CINCINNATI CHILDRENS HOSP MED CTR · PI MADALA, SATISH K · 2013 to 2015
$230k
NHLBI NIH HHS R01 HL082818NHLBI NIH HHS R01 HL111169NHLBI NIH HHS U01 HL101800NIAMS NIH HHS R03 AR062832NIA NIH HHS R21 AG047473
6 · The paper itself

Abstract

Fibrogenesis involves a dynamic interplay between factors that promote the biosynthesis and deposition of extracellular matrix along with pathways that degrade the extracellular matrix and eliminate the primary effector cells. Opposing the often held perception that fibrotic tissue is permanent, animal studies and clinical data now demonstrate the highly plastic nature of organ fibrosis that can, under certain circumstances, regress. This review describes the current understanding of the mechanisms whereby the lung is known to resolve fibrosis focusing on degradation of the extracellular matrix, removal of myofibroblasts, and the role of inflammatory cells. Although there are significant gaps in understanding lung fibrosis resolution, accelerated improvements in biotechnology and bioinformatics are expected to improve the understanding of these mechanisms and have high potential to lead to novel and effective restorative therapies in the treatment not only of pulmonary fibrosis, but also of a wide-ranging spectrum of chronic disorders.

Indexed as

AnimalsCollagenEnzymesExtracellular MatrixHumansLysosomesMiceModels, AnimalProteolysisPulmonary FibrosisCollagenEnzymes

Identifiers

PMID27021937
PMCPMC4861766
OpenAlexW2310526643

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.