Evidence map›Paper›PMID 30118830›Full record

ArticleFree radical biology & medicine2018

Role of GPx3 in PPARγ-induced protection against COPD-associated oxidative stress.

Aravind T Reddy, Sowmya P Lakshmi, Asoka Banno, Raju C Reddy

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

43 citing papers in PubMed, 68 citations in OpenAlex.

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  19. Advances in the role of GPX3 in ovarian cancer (Review).International journal of oncology · 2024
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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

4 authors at 2 institutions in 1 country.

Aravind T ReddyDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, USA.
Sowmya P LakshmiDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, USA.
Asoka BannoDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Raju C ReddyDepartment of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; Veterans Affairs Pittsburgh Healthcare System, Pittsburgh, PA 15240, USA. Electronic address: reddyrc@upmc.edu.
University of Pittsburgh · USVA Pittsburgh Healthcare System · US

Funding

PPAR-delta as a Novel Therapeutic Target in AsthmaR01AI125338 · NIAID · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REDDY, RAJU C · 2016 to 2020
$2.2M
Airway Epithelial Cell Farnesoid X Receptor in COPD PathophysiologyR01HL137842 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REDDY, RAJU C · 2017 to 2019
$1.2M
Role of PPAR-gamma in Smoking-induced COPD Progression and Steroid ResistanceI01BX001102 · VA · VETERANS HEALTH ADMINISTRATION · PI REDDY, RAJU C · 2013 to 2016
–
BLRD VA I01 BX001102NHLBI NIH HHS R01 HL137842NIAID NIH HHS R01 AI125338
6 · The paper itself

Abstract

Cigarette smoke, a source of numerous oxidants, produces oxidative stress and exaggerated inflammatory responses that lead to irreversible lung tissue damage. It is the single, most significant risk factor for chronic obstructive pulmonary disease (COPD). Although an intrinsic defense system that includes both enzymatic and non-enzymatic modulators exists to protect lung tissues against oxidative stress, impairment of these protective mechanisms has been demonstrated in smokers and COPD patients. The antioxidant enzyme GSH peroxidase (GPx) is an important part of this intrinsic defense system. Although cigarette smoke has been shown to downregulate its expression and activity, the underlying mechanism is not known. Peroxisome proliferator-activated receptor γ (PPARγ) is a nuclear hormone receptor with antioxidant effects. PPARγ activation has demonstrated protective effects against cigarette smoke-induced oxidative stress and inflammation. Molecular mechanisms for PPARγ's antioxidant function likewise remain to be elucidated. This study explored the link between PPARγ and GPx3 and found a positive association in cigarette smoke extract (CSE)-exposed human bronchial epithelial cells. Moreover, we provide evidence that identifies GPx3 as a PPARγ transcriptional target. Attenuation of antioxidant effects in the absence of GPx3 highlights the antioxidant's prominent role in mediating PPARγ's function. We also demonstrate that ligand-mediated PPARγ activation blocks CSE-induced reactive oxygen species and hydrogen peroxide production via upregulation of GPx3. In summary, our findings describing the molecular mechanisms involving GPx3 and PPARγ in CSE-induced oxidative stress and inflammation may provide valuable information for the development of more effective therapeutics for COPD.

Indexed as

AntioxidantsBronchiCell LineCigarette SmokingEpithelial CellsGlutathione PeroxidaseHumansOxidative StressPPAR gammaPulmonary Disease, Chronic ObstructiveReactive Oxygen SpeciesSignal TransductionSmokingAntioxidantsGlutathione PeroxidaseGPX3 protein, humanPPAR gammaReactive Oxygen SpeciesAntioxidantCigarette smokeGlutathione (GSH)GSH peroxidasesHuman bronchial epithelial cellsHydrogen peroxide (H(2)O(2))InflammationNF-κBNuclear hormone receptorOxidative stressPPAR response element (PPRE)Reactive oxygen species (ROS)

Identifiers

PMID30118830
PMCPMC6368849
OpenAlexW2887968655

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.