MétaCan
Menu
Back to cohort
Record W2033147946 · doi:10.1089/ars.2010.3829

A Key Role for NOX4 in Epithelial Cell Death During Development of Lung Fibrosis

2011· article· en· W2033147946 on OpenAlexaff
Stéphanie Carnésecchi, Christine Deffert, Yves Donati, Olivier Basset, Boris Hinz, Olivier Preynat‐Seauve, Cécile Guichard, Jack L. Arbiser, Botond Bánfi, Jean‐Claude Pache, Constance Barazzone‐Argiroffo, Karl‐Heinz Krause

Bibliographic record

VenueAntioxidants and Redox Signaling · 2011
Typearticle
Languageen
FieldMedicine
TopicInterstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Canadian institutionsUniversity of Toronto
FundersNational Institute of Arthritis and Musculoskeletal and Skin DiseasesNational Institutes of HealthGertrude von Meissner-Stiftung
KeywordsNOX4BleomycinPulmonary fibrosisFibrosisApoptosisCancer researchBiologyNADPH oxidaseProgrammed cell deathIdiopathic pulmonary fibrosisMyofibroblastOxidative stressInflammationPathogenesisLungHyperoxiaPathologyImmunologyMedicineEndocrinologyInternal medicineBiochemistry

Abstract

fetched live from OpenAlex

UNLABELLED: The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that in lungs of patients with idiopathic lung fibrosis, there is strong expression of NOX4 in hyperplastic alveolar type II cells. AIM: To study a possible causative role of NOX4 in the death of alveolar cells, we have generated NOX4-deficient mice. RESULTS: Three weeks after administration of bleomycin, wild-type (WT) mice developed massive fibrosis, whereas NOX4-deficient mice displayed almost normal lung histology, and only little Smad2 phosphorylation and accumulation of myofibroblasts. However, the protective effects of NOX4 deficiency preceded the fibrotic stage. Indeed, at day 7 after bleomycin, lungs of WT mice showed massive increase in epithelial cell apoptosis and inflammation. In NOX4-deficient mice, no increase in apoptosis was observed, whereas inflammation was comparable to WT. In vitro, NOX4-deficient primary alveolar epithelial cells exposed to transforming growth factor-β(1) did not generate ROS and were protected from apoptosis. Acute treatment with the NOX inhibitors also blunted transforming growth factor-β(1)-induced apoptosis. CONCLUSION: ROS generation by NOX4 is a key player in epithelial cell death leading to pulmonary fibrosis.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.015
GPT teacher head0.238
Teacher spread0.223 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations302
Published2011
Admission routes1
Has abstractyes

Explore more

Same venueAntioxidants and Redox SignalingSame topicInterstitial Lung Diseases and Idiopathic Pulmonary FibrosisFrench-language works237,207