Evidence map›Paper›PMID 35779195›Full record

ReviewInflammation2022

Tight Junctions, the Epithelial Barrier, and Toll-like Receptor-4 During Lung Injury.

Nachiket M Godbole, Asif Alam Chowdhury, Neha Chataut, Shanjana Awasthi

Open access · bronzeAbstract readReview
In one paragraph

Review in Inflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.3field-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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
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  8. Human lung organoids model for assessing host response toFrontiers in cellular and infection microbiology · 2026
    Article
  9. Angiotensin-(1-7) treatment improves pneumonia and prevents sepsis caused by pneumococcal infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Frontiers in allergy · 2025
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

Nachiket M GodboleDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Avenue, Oklahoma City, OK, 73117, USA.
Asif Alam ChowdhuryDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Avenue, Oklahoma City, OK, 73117, USA.
Neha ChatautDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Avenue, Oklahoma City, OK, 73117, USA.
Shanjana AwasthiDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Oklahoma Health Sciences Center, 1110 N. Stonewall Avenue, Oklahoma City, OK, 73117, USA. Shanjana-Awasthi@ouhsc.edu.ORCID http://orcid.org/0000-0003-1249-0708
University of Oklahoma Health Sciences Center · US

Funding

Surfactant protein-A regions as TLR4-immunomodulatorsR01HL136325 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI AWASTHI, SHANJANA · 2017 to 2021
$1.8M
American Association of Immunologists Careers in Immunology Fellowship Application #13916NHLBI NIH HHS R01 HL136325
6 · The paper itself

Abstract

Lung epithelium is constantly exposed to the environment and is critically important for the orchestration of initial responses to infectious organisms, toxins, and allergic stimuli, and maintenance of normal gaseous exchange and pulmonary function. The integrity of lung epithelium, fluid balance, and transport of molecules is dictated by the tight junctions (TJs). The TJs are formed between adjacent cells. We have focused on the topic of the TJ structure and function in lung epithelial cells. This review includes a summary of the last twenty years of literature reports published on the disrupted TJs and epithelial barrier in various lung conditions and expression and regulation of specific TJ proteins against pathogenic stimuli. We discuss the molecular signaling and crosstalk among signaling pathways that control the TJ structure and function. The Toll-like receptor-4 (TLR4) recognizes the pathogen- and damage-associated molecular patterns released during lung injury and inflammation and coordinates cellular responses. The molecular aspects of TLR4 signaling in the context of TJs or the epithelial barrier are not fully known. We describe the current knowledge and possible networking of the TLR4-signaling with cellular and molecular mechanisms of TJs, lung epithelial barrier function, and resistance to treatment strategies.

Indexed as

Lung InjuryTight JunctionsEpithelial CellsEpitheliumHumansToll-Like Receptor 4Toll-Like Receptor 4Barrier functionLung epitheliumTight junctionToll-like receptor-4.

Identifiers

PMID35779195
PMCPMC9649847
OpenAlexW4283774330

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.