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Abstract 4364679: Endothelial ADAM17 is essential in recovery from myocardial infarction by limiting cell death, promoting vascularization and optimizing infarct formation

2025· article· en· W4415793065 on OpenAlexaff
Razoan Al Rimon, Yingxi Li, Ilamaran Meganathan, Faqi Wang, Allan G. Murray, Gavin Y. Oudit, Slava Epelman, Xavier Clemente‐Casares, Zamaneh Kassiri

Bibliographic record

VenueCirculation · 2025
Typearticle
Languageen
FieldMedicine
TopicCardiac Fibrosis and Remodeling
Canadian institutionsUniversity Health NetworkUniversity of Alberta
Fundersnot available
KeywordsMyocardial infarctionEndothelial stem cellLigationApoptosisImmune systemCardiac function curveTroponin complexEndotheliumVentricular remodeling

Abstract

fetched live from OpenAlex

Introduction: Myocardial infarction (MI) is a leading cause of death worldwide, and endothelial cells (ECs) are central to the repair process by coordinating angiogenesis, immune cell recruitment, and endothelial-to-mesenchymal transition (EndMT). ADAM17, a membrane-bound protease elevated in cardiovascular disease, regulates multiple cellular processes through ectodomain shedding of different molecules. However, the causal role of endothelial ADAM17 in post-MI recovery remains poorly defined. Methods: Male and female mice with inducible endothelial-specific ADAM17 knockdown ( Adam17 f/f / Cdhr5 Cre ERT ; Adam17 EC-KD ) and control cohorts ( Adam17 f/f , Cdhr5 Cre ERT , WT) underwent left anterior descending coronary artery ligation to induce experimental MI. Cardiac structure and function were evaluated (echocardiography), histological analyses (Trichrome staining), molecular analyses (immunofluorescent staining (IF), western blotting, and single-nucleus RNA sequencing (snRNA-seq)) at various post-MI time points. Results: Adam17 EC-KD mice exhibited reduced post-MI survival (increased LV rupture), increased left ventricular rupture, and progressive decline in cardiac function with reduced ejection fraction. Adam17 EC-KD mice exhibited increased neutrophil infiltration, NETosis, and cytotoxic T cell accumulation at 1 day post-MI; however, depletion of any of these immune cells further exacerbated the post-MI mortality (due to LV rupture), highlighting their potential protective contribution. Loss of endothelial ADAM17 resulted in decreased coronary density in the infarct myocardium (CD31 IF; 3-D micro-CT imaging), with reduced pVEGFR2 signaling, suggesting impaired angiogenesis. In addition, SnRNA-seq confirmed the suppressed pro-angiogenic pathways, and identified an endothelial cell subpopulation enriched for necroptotic markers, displaying increased ligand-receptor interactions with inflammatory macrophages. Mechanistically, endothelial ADAM17 deficiency enhanced necroptotic cell death via activation of the TNFR1-RIP3K-RIP1K-MLKL axis. Adam17 EC-KD hearts also showed impaired collagen crosslinking and reduced activation of the SMAD pathway (pSMAD2/3), lysyl oxidase, and Fibronectin expression, indicating defective EndMT, supported by reduced EndMT gene signatures in snRNA-seq. Conclusion: Endothelial ADAM17 is essential for effective post-MI cardiac repair by regulating endothelial survival, angiogenesis, immune cell infiltration, and infarct formation.

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 distilled prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. Learned from the 10,348 direct Codex labels and 10,348 direct Gemma labels. Candidate is the union of thresholded teacher heads; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels or direct frontier model labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: codex-gemma-dda1882f352aValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: none
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.793
Threshold uncertainty score0.698

Codex and Gemma teacher scores by category

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 communication0.0000.001
Open science0.0000.000
Research integrity0.0000.000
Insufficient payload (model declined to judge)0.0000.000

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 head0.010
GPT teacher head0.236
Teacher spread0.226 · 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 teacher head, 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
Published2025
Admission routes1
Has abstractyes

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