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Defining the Aryl Hydrocarbon Receptor as a Driver of Pulmonary Fibrosis

2025· article· en· W4410273114 on OpenAlexaff
Willem Rijnbout St. James, Emily Wilson, Étienne Marcotte, Jieping Ding, Parameswaran Nair, David H. Eidelman, Carolyn J. Baglole

Bibliographic record

VenueAmerican Journal of Respiratory and Critical Care Medicine · 2025
Typearticle
Languageen
FieldMedicine
TopicChronic Obstructive Pulmonary Disease (COPD) Research
Canadian institutionsChristie (Canada)McMaster UniversityMcGill University
Fundersnot available
KeywordsAryl hydrocarbon receptorMedicineArylHydrocarbonPulmonary fibrosisFibrosisInternal medicineOrganic chemistryBiochemistry

Abstract

fetched live from OpenAlex

Abstract Rationale: Idiopathic pulmonary fibrosis (IPF) is the most common and severe interstitial lung disease (ILD), carrying a median survival of 3 years after diagnosis. In IPF, dysregulation of signaling pathways involved in extracellular matrix (ECM) production, such as transforming growth factor-β (TGF-β) signaling, lead to persistent activation of lung fibroblasts and results in the overproduction of ECM proteins such as collagen. We hypothesized that the aryl hydrocarbon receptor (AhR), a transcription factor originally characterized as a mediator of xenobiotic metabolism, is mechanistically involved in the development of fibrosis. To address this hypothesis, we evaluated the role of the AhR in fibroblast-mediated fibrotic outcomes in in-vitro and in-vivo models of pulmonary fibrosis. Methods: Primary mouse lung fibroblasts (MLFs) from AhR wild-type (Ahr+/+) and AhR knock-out (Ahr-/-) mice were treated with TGF-β (5 ng/mL) for 48 hours with or without the AhR inhibitor CH223191 (10µM). Collagen 1A1 (Col1a1) and α-smooth muscle actin (α-SMA) protein were measured via immunoblot. We performed proteomic analysis of cell lysate from Ahr+/+ and Ahr-/- MLFs treated with or without TGF-β via liquid chromatography-mass spectrometry (LC/MS). As a complement, the AhR was also knocked down in primary human lung fibroblasts (HLFs) using AhR-targeting siRNA. TGF-β-stimulated Col1a1 production was then evaluated via immunoblot. To evaluate AhR-dependency of pulmonary fibrosis in-vivo, Ahr+/+ and Ahr-/- mice were treated with bleomycin (2 mg/kg) via oropharyngeal administration and lung collagen deposition was evaluated 21 days later via Masson's Trichrome and quantified with hydroxyproline assay. Results: Col1a1 protein is reduced in Ahr-/- MLFs compared to Ahr+/+ controls both at baseline and in response to TGF-β. CH223191 attenuated TGF-β-stimulated Col1a1 production by Ahr+/+ MLFs. HLFs treated with AhR-targeting siRNA have reduced Col1a1 production compared to cells treated with siRNA controls. Proteomic analysis revealed reduced levels of proteins involved in collagen biosynthesis (Serpinh1, Plod3, Mia3, Colgalt1, Crtap, Ph31), actin polymerization (Cotl1, Arap1, Stmn1, Swap70, Flna), and mechanotransduction (Thy1, Rhog, Itga5, Itgb5) in AhR-deficient cells. Furthermore, Ahr-/- mice appear to be resistant to bleomycin-induced pulmonary fibrosis compared to Ahr+/+ controls. Conclusions: Our findings suggest that the AhR is essential for the development of the fibrotic phenotype in in-vitro and in-vivo models of pulmonary fibrosis. Future work will determine whether AhR antagonism can reverse the fibrotic phenotype, aiming to establish a novel therapeutic approach for combating 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 score0.001
Threshold uncertainty score0.005

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 integrity0.0010.001
Insufficient payload (model declined to judge)0.0010.000

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 head0.011
GPT teacher head0.317
Teacher spread0.306 · 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

Citations0
Published2025
Admission routes1
Has abstractyes

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