Evidence map›Paper›PMID 30098327›Full record

ReviewMolecular aspects of medicine2018

Oxidative stress in chronic lung disease: From mitochondrial dysfunction to dysregulated redox signaling.

Albert van der Vliet, Yvonne M W Janssen-Heininger, Vikas Anathy

Open access · greenAbstract readReview
In one paragraph

Review in Molecular aspects of medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

93 citing papers in PubMed, 158 citations in OpenAlex.

  1. Trial
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  5. Bicyclol: A Useful Agent for Silicosis?International journal of molecular sciences · 2026
    Review
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  10. Loss of PIK3CA allowsbioRxiv : the preprint server for biology · 2026
    Article
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  20. A Redox-Shifted Fibroblast Subpopulation Emerges in the Fibrotic Lung.American journal of respiratory cell and molecular biology · 2024
    Article

33 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

3 authors at 1 institution in 1 country.

Albert van der VlietDepartment of Pathology and Laboratory Medicine, Vermont Lung Center, Larner College of Medicine, University of Vermont, Burlington, VT, 05405, USA. Electronic address: albert.van-der-vliet@uvm.edu.
Yvonne M W Janssen-HeiningerDepartment of Pathology and Laboratory Medicine, Vermont Lung Center, Larner College of Medicine, University of Vermont, Burlington, VT, 05405, USA.
Vikas AnathyDepartment of Pathology and Laboratory Medicine, Vermont Lung Center, Larner College of Medicine, University of Vermont, Burlington, VT, 05405, USA.
University of Vermont · US

Funding

VERMONT IMMUNOBIOLOIGY/ INFECTIOUS DISEASES CENTERP20RR021905 · NCRR · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2006 to 2011
$14.5M
Vermont Immunology/Infectious Diseases CenterP30GM118228 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BUDD, RALPH C · 2016 to 2021
$6.8M
S-glutathionylation chemistry in fibrotic lung remodelingR35HL135828 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI JANSSEN-HEININGER, YVONNE M. W. · 2017 to 2023
$6.5M
Dual Oxidase in Airway Epithelial Repair and RemodelingR01HL085646 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2008 to 2020
$4.7M
Endoplasmic Reticulum Stress Signaling in Allergen-induced Airway RemodelingR01HL122383 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI ANATHY, VIKAS · 2015 to 2023
$3.5M
S-glutathionylation chemistry, glycolysis and obese allergic asthmaR01HL137268 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI DIXON, ANNE E, VAN DER VLIET, ALBERT · 2017 to 2020
$2.1M
DUOX1 and Mitochondria in Obese AsthmaR01HL138708 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2017 to 2020
$2.1M
DUOX1 Silencing in Age-Related COPDR21AG055325 · NIA · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI VAN DER VLIET, ALBERT · 2017 to 2018
$429k
NCRR NIH HHS P20 RR021905NHLBI NIH HHS R01 HL085646NHLBI NIH HHS R01 HL122383NHLBI NIH HHS R01 HL137268NHLBI NIH HHS R01 HL138708NHLBI NIH HHS R35 HL135828NIA NIH HHS R21 AG055325NIGMS NIH HHS P30 GM118228
6 · The paper itself

Abstract

The lung is a delicate organ with a large surface area that is continuously exposed to the external environment, and is therefore highly vulnerable to exogenous sources of oxidative stress. In addition, each of its approximately 40 cell types can also generate reactive oxygen species (ROS), as byproducts of cellular metabolism and in a more regulated manner by NOX enzymes with functions in host defense, immune regulation, and cell proliferation or differentiation. To effectively regulate the biological actions of exogenous and endogenous ROS, various enzymatic and non-enzymatic antioxidant defense systems are present in all lung cell types to provide adequate protection against their injurious effects and to allow for appropriate ROS-mediated biological signaling. Acute and chronic lung diseases are commonly thought to be associated with increased oxidative stress, evidenced by altered cellular or extracellular redox status, increased irreversible oxidative modifications in proteins or DNA, mitochondrial dysfunction, and altered expression or activity of NOX enzymes and antioxidant enzyme systems. However, supplementation strategies with generic antioxidants have been minimally successful in prevention or treatment of lung disease, most likely due to their inability to distinguish between harmful and beneficial actions of ROS. Recent studies have attempted to identify specific redox-based mechanisms that may mediate chronic lung disease, such as allergic asthma or pulmonary fibrosis, which provide opportunities for selective redox-based therapeutic strategies that may be useful in treatment of these diseases.

Indexed as

Oxidative StressAnimalsBiomarkersChronic DiseaseHumansLung DiseasesMitochondriaOxidation-ReductionReactive Oxygen SpeciesSignal TransductionBiomarkersReactive Oxygen SpeciesAsthmaEpitheliumER stressFibrosisNOXS-glutathionylationSulfenylation

Identifiers

PMID30098327
PMCPMC6181583
OpenAlexW2888427456

What OpenQuestion holds

Textmetadata
LicenceTDM
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.