Evidence map›Paper›PMID 27921210›Full record

ReviewPflugers Archiv : European journal of physiology2017

Tight junctions in pulmonary epithelia during lung inflammation.

Oliver H Wittekindt

Abstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

114 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
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  4. Article
  5. Review
  6. [A prediction model for refractory pneumonia in children based on early lung ultrasound findings].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  7. Article
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  11. Observational
  12. 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
  13. Review
  14. Article
  15. Article
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  17. Article
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54 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

1 author.

Oliver H WittekindtInstitute of General Physiology, Ulm University, Albert-Einstein-Allee 11, 89081, Ulm, Germany. oliver.wittekindt@uni-ulm.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory lung diseases like asthma bronchiale, chronic obstructive pulmonary disease and allergic airway inflammation are widespread public diseases that constitute an enormous burden to the health systems. Mainly classified as inflammatory diseases, the treatment focuses on strategies interfering with local inflammatory responses by the immune system. Inflammatory lung diseases predispose patients to severe lung failures like alveolar oedema, respiratory distress syndrome and acute lung injury. These life-threatening syndromes are caused by increased permeability of the alveolar and airway epithelium and exudate formation. However, the mechanism underlying epithelium barrier breakdown in the lung during inflammation is elusive. This review emphasises the role of the tight junction of the airway epithelium as the predominating structure conferring epithelial tightness and preventing exudate formation and the impact of inflammatory perturbations on their function.

Indexed as

AnimalsEpitheliumHumansLungPermeabilityPneumoniaTight JunctionsARDSAsthmaCOPDInflammationLungTight junctions

Identifiers

PMID27921210
PMCPMC5203840

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.