Evidence map›Paper›PMID 24142519›Full record

ReviewAmerican journal of physiology. Lung cellular and molecular physiology2013

The Witschi Hypothesis revisited after 35 years: genetic proof from SP-C BRICHOS domain mutations.

Bruce D Uhal, Hang Nguyen

Abstract readReview
In one paragraph

Review in American journal of physiology. Lung cellular and molecular physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Systematic review of drug effects in humans and models with surfactant-processing disease.European respiratory review : an official journal of the European Respiratory Society · 2018
    Pooled it
  2. Article
  3. Genetic disorders of the surfactant system: focus on adult disease.European respiratory review : an official journal of the European Respiratory Society · 2021
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. SIRT3 deficiency promotes lung fibrosis by augmenting alveolar epithelial cell mitochondrial DNA damage and apoptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  11. Review
  12. Article
  13. Article
  14. Using electron microscopes to look into the lung.Histochemistry and cell biology · 2016
    Review
  15. Article
  16. Article
  17. Review
  18. Targeted Type 2 Alveolar Cell Depletion. A Dynamic Functional Model for Lung Injury Repair.American journal of respiratory cell and molecular biology · 2016
    Article
  19. Review
  20. Review
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.

Bruce D UhalDept. of Physiology, Michigan State Univ., 3197 Biomedical and Physical Sciences Bldg., East Lansing, MI 48824. uhal@msu.edu.
Hang Nguyen
Michigan State University · US

Funding

CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR01HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1996 to 2012
$2.9M
CONTROL OF TYPE II PNEUMOCYTE PROLIFERATIONR29HL045136 · NHLBI · RUSH UNIVERSITY MEDICAL CENTER · PI UHAL, BRUCE D · 1990 to 1994
–
NHLBI NIH HHS HL-45136
6 · The paper itself

Abstract

Over 35 years ago, Wanda Haschek and Hanspeter Witschi published a theory for the pathogenesis of lung fibrosis that dared to challenge the longstanding view of lung fibrosis as an "inflammatory disease." On the basis of considerable experimental evidence, they proposed that lung fibrosis was initiated and propagated by microfoci of epithelial damage that, if unrepaired, upset the normal epithelial-fibroblast balance to create profibrotic microenvironments, without any obligatory contribution of "inflammatory" cells. Unfortunately, this theory was largely overlooked for many years. In the meantime, the repeated failure of attempts to treat idiopathic pulmonary fibrosis with anti-inflammatory regimens has led some investigators to revive the theory referred to, in decades past, as "The Witschi Hypothesis." This manuscript briefly reviews more recent evidence in support of the "Severity of Epithelial Injury" Hypothesis proposed by Haschek and Witschi. More important, it offers the updated viewpoint that mutations in the BRICHOS domain of surfactant protein C, which cause interstitial lung disease and induce cell death specifically in lung epithelial cells, in effect provide genetic proof that the Witschi Hypothesis is indeed the correct theory to explain the pathogenesis of fibrosis in the lungs.

Indexed as

AnimalsEpithelial CellsHumansMutationProtein Structure, TertiaryPulmonary AlveoliPulmonary FibrosisPulmonary Surfactant-Associated ProteinsPulmonary Surfactant-Associated Proteinsalveolar epithelial cellsepithelial-mesenchymal cross talkidiopathic pulmonary fibrosislung fibrosistype II pneumocyte

Identifiers

PMID24142519
PMCPMC3882532
OpenAlexW2316098036

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.