Evidence map›Paper›PMID 27233996›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2016

Alveolar epithelial disintegrity in pulmonary fibrosis.

Tejaswini Kulkarni, Joao de Andrade, Yong Zhou, Tracy Luckhardt, Victor J Thannickal

Open access · greenAbstract readCase ReportsReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 6% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  6. Evidence for a lipofibroblast-to-The European respiratory journal · 2025
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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

5 authors at 1 institution in 1 country.

Tejaswini KulkarniDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama.ORCID http://orcid.org/0000-0002-4251-4988
Joao de AndradeDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Yong ZhouDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Tracy LuckhardtDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
Victor J ThannickalDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Alabama at Birmingham, Birmingham, Alabama vjthan@uab.edu.
University of Alabama at Birmingham · US

Funding

Therapeutic Targeting of the Myofibroblast in Fibrotic Lung DiseaseP01HL114470 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2013 to 2022
$17.8M
Myofibroblast Senescence in Pulmonary FibrosisR01AG046210 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THANNICKAL, VICTOR J. · 2014 to 2018
$1.6M
The Role of Biomechanical Signaling in Lung FibrosisR01HL124076 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHOU, YONG · 2015 to 2018
$1.5M
Sirtuins in Lung Aging and FibrosisI01BX003056 · VA · SOUTHEAST LOUISIANA VETERANS HEALTH CARE · PI THANNICKAL, VICTOR J. · 2016 to 2025
–
BLRD VA I01 BX003056NHLBI NIH HHS P01 HL114470NHLBI NIH HHS R01 HL124076NIA NIH HHS R01 AG046210
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease characterized by progressive decline in lung function, resulting in significant morbidity and mortality. Current concepts of the pathogenesis of IPF primarily center on dysregulated epithelial cell repair and altered epithelial-mesenchymal communication and extracellular matrix deposition following chronic exposure to cigarette smoke or environmental toxins. In recent years, increasing attention has been directed toward the role of the intercellular junctional complex in determining the specific properties of epithelia in pulmonary diseases. Additionally, recent genomewide association studies suggest that specific genetic variants predictive of epithelial cell dysfunction may confer susceptibility to the development of sporadic idiopathic pulmonary fibrosis. A number of genetic disorders linked to pulmonary fibrosis and familial interstitial pneumonias are associated with loss of epithelial integrity. However, the potential links between extrapulmonary clinical syndromes associated with defects in epithelial cells and the development of pulmonary fibrosis are not well understood. Here, we report a case of hereditary mucoepithelial dysplasia that presented with pulmonary fibrosis and emphysema on high-resolution computed tomography. This case illustrates a more generalizable concept of epithelial disintegrity in the development of fibrotic lung diseases, which is explored in greater detail in this review article.

Indexed as

AdultAlveolar Epithelial CellsCell CommunicationGenetic Predisposition to DiseaseHumansIdiopathic Pulmonary FibrosisMaleTomography, X-Ray Computedcell-cell adhesionepithelial barrier dysfunctionepithelial junctional complexpulmonary fibrosis

Identifiers

PMID27233996
PMCPMC5005273
OpenAlexW2398822735

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.