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Abstract 15608: Atp Citrate Lyase a New Signaling Hub Between Metabolism and Epigenetic in Vascular Remodeling and Right Ventricle Failure in Pulmonary Arterial Hypertension

2020· article· en· W3160152163 on OpenAlexaff
Charlotte Romanet, Alice Bourgeois, Yann Grobs, Sandra Breuils Bonnet, Valérie Nadeau, Steeve Provencher, Olivier Boucherat, Sébastien Bonnet

Bibliographic record

VenueCirculation · 2020
Typearticle
Languageen
FieldMedicine
TopicPulmonary Hypertension Research and Treatments
Canadian institutionsUniversité LavalInstitut universitaire de cardiologie et de pneumologie de Québec
Fundersnot available
KeywordsDownregulation and upregulationMedicineCancer researchATP citrate lyaseVascular remodelling in the embryoEndocrinologyCell biologyInternal medicineBiologyCitrate synthaseBiochemistry

Abstract

fetched live from OpenAlex

Objective: Pulmonary arterial hypertension (PAH) is a lung disease characterized by vascular lesions and obstruction of distal pulmonary arteries (PA) leading to right ventricle (RV) remodeling and death. Similar to cancer cells, PA smooth muscle cells (PASMCs) exhibit an excessive proliferation and resistance to apoptosis, pivot components of vascular remodeling, due to epigenetic reprogramming and Warburg effect. This epigenetic/metabolic signature is attributed in part to the upregulation of ATP citrate lyase (ACLY). By decreasing cytosolic levels of citrate, ACLY supports glycolysis, while by generating acetyl-coA in the nucleus it promotes histone acetylation and signaling pathways supporting pathological processes like proliferation, hypertrophy, and fibrosis, pathological features in PAH. In the cytosol, ACLY controls the synthesis of lipids required for proliferating cells to generate membranes. We thus hypothesized that ACLY is upregulated in PAH and contributes to PA remodeling and RV failure. Methods/Results: Using immunoblot, we showed an upregulation of ACLY in human distal PA and isolated PASMCs from PAH patients (p<0.05 ; n=10), like in Sugen/Hypoxia rat model. In vitro, pharmacological inhibition of ACLY significantly decreased PAH-PASMC proliferation (Ki67 labeling), resistance to apoptosis (Annexin V and caspase 3 assays) and restored a proper metabolism (seahorse assay) (p<0.05 ; n=5). Mechanistically, we showed that ACLY inhibition decreases P300-dependent pro-survival factors including Survivin, PCNA, cMYC, PKM2, phospho-PDH / PDH, and restores FOXO3 and AMPK functions know to be decreased in PAH. Besides, we found that ACLY expression was upregulated in failed RV from rats subjected to pulmonary artery banding; its expression correlating negatively with stroke volume and positively with RVEDP; hypertrophy and fibrosis. Conclusion: Our preliminary data suggest that ACLY contributes to vascular remodeling in PAH. Current experiments aim to demonstrate whether 1) pharmacological inhibition of ACLY reverses PAH in animal models and 2) whether inactivation of Acly targeted to smooth muscle cells and cardiomyocytes improves pulmonary vascular remodeling and RV dysfunction, respectively.

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 score0.016
Threshold uncertainty score0.054

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0010.001
Open science0.0000.000
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0160.005

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 head0.040
GPT teacher head0.260
Teacher spread0.220 · 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".

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Citations0
Published2020
Admission routes1
Has abstractyes

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