Evidence map›Paper›PMID 29026006›Full record

ReviewBioscience reports2017

Potential contribution of alveolar epithelial type I cells to pulmonary fibrosis.

Michael Kasper, Kathrin Barth

Open access · goldAbstract readReview
In one paragraph

Review in Bioscience reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
6.3field-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

54 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. Review
  3. Frontiers in pharmacology · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Immunobiology of pulmonary fibrosis.Frontiers in immunology · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  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.

Michael KasperMedical Faculty 'Carl Gustav Carus', Institute of Anatomy, Technical University of Dresden, Fetscherstr. 74, Dresden D-01307, Germany.
Kathrin BarthMedical Faculty 'Carl Gustav Carus', Institute of Anatomy, Technical University of Dresden, Fetscherstr. 74, Dresden D-01307, Germany michael.kasper@tu-dresden.de.
Carl Gustav Carus-Institut · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is characterized by inflammation and fibrosis of the interstitium and destruction of alveolar histoarchitecture ultimately leading to a fatal impairment of lung function. Different concepts describe either a dominant role of inflammatory pathways or a disturbed remodeling of resident cells of the lung parenchyma during fibrogenesis. Further, a combination of both the mechanisms has been postulated. The present review emphasizes the particular involvement of alveolar epithelial type I cells in all these processes, their contribution to innate immune/inflammatory functions and maintenance of proper alveolar barrier functions. Amongst the different inflammatory and repair events the purinergic receptor P2X7, an ATP-gated cationic channel that regulates not only apoptosis, necrosis, autophagy, and NLPR3 inflammosome activation, but also the turnover of diverse tight junction (TJ) and water channel proteins, seems to be essential for the stability of alveolar barrier integrity and for the interaction with protective factors during lung injury.

Indexed as

Alveolar Epithelial CellsAnimalsApoptosisAquaporinsAutophagyHumansImmunity, InnateInflammationMiceNecrosisPulmonary FibrosisReceptors, Purinergic P2X7Tight JunctionsAquaporinsP2RX7 protein, humanReceptors, Purinergic P2X7alveolar epithelial type I cellP2X7Rpulmonary fibrosis

Identifiers

PMID29026006
PMCPMC5696455
OpenAlexW2761923461

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.