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Record W4412160653 · doi:10.1183/13993003.02250-2024

Pharmacological inhibition of Epac1 protects against pulmonary fibrosis by blocking FoxO3a neddylation

2025· article· en· W4412160653 on OpenAlexaff
Katherine Jankowski, Sarah E Lemay, Daniel Lozano-Ojalvo, Leticia Pérez‐Rodríguez, Mélanie Sauvaget, Sandra Breuils‐Bonnet, Karina Formoso, Vineeta Jagana, M. F. Ochoa, Shihong Zhang, Javier Milara, Julio Cortijo, Irene C. Turnbull, Steeve Provencher, Sébastien Bonnet, Jordi Ochando, Frank Lezoualc’h, Malik Bisserier, Lahouaria Hadri

Bibliographic record

VenueEuropean Respiratory Journal · 2025
Typearticle
Languageen
FieldMedicine
TopicInterstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Canadian institutionsUniversité LavalInstitut universitaire de cardiologie et de pneumologie de Québec
FundersNational Center for Advancing Translational SciencesNational Institutes of HealthAgence Nationale de la RechercheNational Heart, Lung, and Blood InstituteAmerican Lung AssociationAmerican Thoracic SocietyFondation pour la Recherche MédicaleAmerican Heart Association
KeywordsMedicineNeddylationBlocking (statistics)Pulmonary fibrosisPharmacologyFibrosisInternal medicineUbiquitinBiochemistry

Abstract

fetched live from OpenAlex

Background Idiopathic pulmonary fibrosis (IPF) is marked by progressive lung scarring with no existing cure, emphasising the need for new therapeutic targets. Current evidence suggests that cyclic adenosine monophosphate (cAMP) mitigates lung fibroblast proliferation via the protein kinase A pathway, but the impact of exchange proteins directly activated by cAMP 1 (Epac1) on IPF remains unexplored. Objective To investigate the role of Epac1 in IPF progression. Methods We examined lung samples from IPF patients and controls, and from a bleomycin-induced mouse model of pulmonary fibrosis. The effects of Epac were analysed in knockout mice and through modulation using viral vectors. The Epac1-specific small compound inhibitor AM-001 was evaluated in vitro using lung fibroblasts from patients with IPF, in vivo in bleomycin mice and ex vivo in IPF precision-cut lung slices. Results Increased Epac1 expression was observed in lung tissues from IPF patients, fibrotic fibroblasts and bleomycin-challenged mice. Genetic or pharmacological inhibition of Epac1 with AM-001 decreased proliferation in normal and IPF fibroblasts, and reduced expression of profibrotic markers such as α-smooth muscle actin, transforming growth factor-β/SMAD family member 2/3, and interleukin-6/signal transducer and activator of transcription 3 pathways. Epac1-specific inhibition consistently protected against bleomycin-induced lung injury and fibrosis, suggesting significant therapeutic potential. Global gene expression profiling indicated a reduced profibrotic gene signature and neddylation pathway components in Epac1-deficient fibroblasts and human-derived lung cells. Mechanistically, the protective effects may involve inhibiting the neddylation pathway and preventing neural precursor cell expressed, developmentally downregulated 8 (NEDD8) activation, which in turn reduces the degradation of forkhead box protein O3 by NEDD8. Additionally, these effects may be enhanced while also limiting the proliferation of lung-infiltrating monocytes. Conclusions Our findings demonstrate that Epac1 regulates fibroblast activity in pulmonary fibrosis, and that targeting Epac1 with the pharmacological specific inhibitor AM-001 offers a promising therapeutic approach for treating IPF disease.

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 score0.008

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 integrity0.0000.001
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 head0.277
Teacher spread0.262 · 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

Citations5
Published2025
Admission routes1
Has abstractyes

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