Evidence map›Paper›PMID 36830000›Full record

ArticleAntioxidants (Basel, Switzerland)2023

Differences in Treatment Response in Bronchial Epithelial Cells from Idiopathic Pulmonary Fibrosis (IPF) Patients: A First Step towards Personalized Medicine?

C Veith, M A Schneider, L Maas, A van der Vliet, F J van Schooten, M Kreuter, M Meister, A W Boots, N Kahn

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 3 institutions in 3 countries.

C VeithDepartment of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Faculty Health, Medicine and Life Sciences, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
M A SchneiderTranslational Lung Research Unit, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany.ORCID 0000-0001-8269-3821
L MaasDepartment of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Faculty Health, Medicine and Life Sciences, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
A van der VlietDepartment of Pathology & Laboratory Medicine, Larner College of Medicine, University of Vermont, Burlington, VT 05405, USA.
F J van SchootenDepartment of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Faculty Health, Medicine and Life Sciences, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
M KreuterTranslational Lung Research Center Heidelberg, 69120 Heidelberg, Germany.
M MeisterTranslational Lung Research Unit, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany.
A W BootsDepartment of Pharmacology and Toxicology, NUTRIM School of Nutrition, Translational Research and Metabolism, Faculty Health, Medicine and Life Sciences, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands.ORCID 0000-0003-0138-0124
N KahnTranslational Lung Research Unit, Thoraxklinik, Heidelberg University Hospital, 69126 Heidelberg, Germany.
Heidelberg University · DEMaastricht University · NLUniversity of Vermont · US

Funding

Lung Foundation Netherlands 9.2.17.214FE
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) has a detrimental prognosis despite antifibrotic therapies to which individual responses vary. IPF pathology is associated with oxidative stress, inflammation and increased activation of SRC family kinases (SFK). This pilot study evaluates individual responses to pirfenidone, nintedanib and SFK inhibitor saracatinib, markers of redox homeostasis, fibrosis and inflammation, in IPF-derived human bronchial epithelial (HBE) cells. Differentiated HBE cells from patients with and without IPF were analyzed for potential alterations in redox and profibrotic genes and pro-inflammatory cytokine secretion. Additionally, the effects of pirfenidone, nintedanib and saracatinib on these markers were determined. HBE cells were differentiated into a bronchial epithelium containing ciliated epithelial, basal, goblet and club cells. NOX4 expression was increased in IPF-derived HBE cells but differed on an individual level. In patients with higher NOX4 expression, pirfenidone induced antioxidant gene expression. All drugs significantly decreased NOX4 expression. IL-6 (

Indexed as

IPFnintedanibpersonalized medicinepirfenidoneprimary bronchial epithelial cellssaracatinib

Identifiers

PMID36830000
PMCPMC9952618
OpenAlexW4319968893

What OpenQuestion holds

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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.