Evidence map›Paper›PMID 26150910›Full record

ReviewJournal of thoracic disease2015

Pleural mesothelial cells in pleural and lung diseases.

Hitesh Batra, Veena B Antony

Abstract readReview
In one paragraph

Review in Journal of thoracic disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
7.1field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Ventilator-induced Lung Injury Promotes Inflammation within the Pleural Cavity.American journal of respiratory cell and molecular biology · 2024
    Article
  10. Myocardin regulates fibronectin expression and secretion from human pleural mesothelial cells.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  11. Role of ZIP kinase in development of myofibroblast differentiation from HPMCs.American journal of physiology. Lung cellular and molecular physiology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Journal of clinical medicine · 2022
    Review
  18. DOCK-t(w)o Pleural Fibrosis.American journal of respiratory cell and molecular biology · 2022
    Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Hitesh BatraDivision of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham Birmingham, AL, USA.
Veena B AntonyDivision of Pulmonary, Allergy & Critical Care Medicine, Department of Medicine, University of Alabama at Birmingham Birmingham, AL, USA.
University of Alabama at Birmingham · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During development, the mesoderm maintains a complex relationship with the developing endoderm giving rise to the mature lung. Pleural mesothelial cells (PMCs) derived from the mesoderm play a key role during the development of the lung. The pleural mesothelium differentiates to give rise to the endothelium and smooth muscle cells via epithelial-to-mesenchymal transition (EMT). An aberrant recapitulation of such developmental pathways can play an important role in the pathogenesis of disease processes such as idiopathic pulmonary fibrosis (IPF). The PMC is the central component of the immune responses of the pleura. When exposed to noxious stimuli, it demonstrates innate immune responses such as Toll-like receptor (TLR) recognition of pathogen associated molecular patterns as well as causes the release of several cytokines to activate adaptive immune responses. Development of pleural effusions occurs due to an imbalance in the dynamic interaction between junctional proteins, n-cadherin and β-catenin, and phosphorylation of adherens junctions between PMCs, which is caused in part by vascular endothelial growth factor (VEGF) released by PMCs. PMCs play an important role in defense mechanisms against bacterial and mycobacterial pleural infections, and in pathogenesis of malignant pleural effusion, asbestos related pleural disease and malignant pleural mesothelioma. PMCs also play a key role in the resolution of inflammation, which can occur with or without fibrosis. Fibrosis occurs as a result of disordered fibrin turnover and due to the effects of cytokines such as transforming growth factor-β, platelet-derived growth factor (PDGF), and basic fibroblast growth factor; which are released by PMCs. Recent studies have demonstrated a role for PMCs in the pathogenesis of IPF suggesting their potential as a cellular biomarker of disease activity and as a possible therapeutic target. Pleural-based therapies targeting PMCs for treatment of IPF and other lung diseases need further exploration.

Indexed as

epithelial-mesenchymal transition (EMT)idiopathic pulmonary fibrosis (IPF)pleural mesothelial cells (PMCs)Pleural mesothelium1Wilms tumor-1 (WT1)

Identifiers

PMID26150910
PMCPMC4466423
OpenAlexW1942297034

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.