Evidence map›Paper›PMID 35344036›Full record

ArticleDisease models & mechanisms2022

Dysregulated mitochondrial metabolism upon cigarette smoke exposure in various human bronchial epithelial cell models.

Christy B M Tulen, Ying Wang, Daan Beentjes, Phyllis J J Jessen, Dennis K Ninaber, Niki L Reynaert, Frederik-Jan van Schooten, Antoon Opperhuizen, Pieter S Hiemstra, Alexander H V Remels

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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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

10 authors at 2 institutions in 2 countries.

Christy B M TulenDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.ORCID 0000-0002-2537-3036
Ying WangDepartment of Pulmonology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Daan BeentjesDepartment of Pulmonology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Phyllis J J JessenDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.
Dennis K NinaberDepartment of Pulmonology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Niki L ReynaertDepartment of Respiratory Medicine, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.
Frederik-Jan van SchootenDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.
Antoon OpperhuizenDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.
Pieter S HiemstraDepartment of Pulmonology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands.
Alexander H V RemelsDepartment of Pharmacology and Toxicology, School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Center+, PO Box 616, 6200 MD Maastricht, The Netherlands.
University Medical Center · USLeiden University Medical Center · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure to cigarette smoke (CS) is the primary risk factor for developing chronic obstructive pulmonary disease. The impact of CS exposure on the molecular mechanisms involved in mitochondrial quality control in airway epithelial cells is incompletely understood. Undifferentiated or differentiated primary bronchial epithelial cells were acutely/chronically exposed to whole CS (WCS) or CS extract (CSE) in submerged or air-liquid interface conditions. Abundance of key regulators controlling mitochondrial biogenesis, mitophagy and mitochondrial dynamics was assessed. Acute exposure to WCS or CSE increased the abundance of components of autophagy and receptor-mediated mitophagy in all models. Although mitochondrial content and dynamics appeared to be unaltered in response to CS, changes in both the molecular control of mitochondrial biogenesis and a shift toward an increased glycolytic metabolism were observed in particular in differentiated cultures. These alterations persisted, at least in part, after chronic exposure to WCS during differentiation and upon subsequent discontinuation of WCS exposure. In conclusion, smoke exposure alters the regulation of mitochondrial metabolism in airway epithelial cells, but observed alterations may differ between various culture models used. This article has an associated First Person interview with the joint first authors of the paper.

Indexed as

Cigarette SmokingPulmonary Disease, Chronic ObstructiveBronchiEpithelial CellsHumansMitochondriaMitophagyNicotianaAutophagyCell modelCigarette smokeCulture methodsHuman primary bronchial epithelial cellsMitochondrial metabolism

Identifiers

PMID35344036
PMCPMC8990921
OpenAlexW4220709565

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.