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Activation of AMPK via inhibition of PAR2 limits myocardial ischemia-reperfusion injury

2025· article· en· W7127598356 on OpenAlexaff
L I S H A Li, Y A D A N Qi, L H Young, D A K E Qi

Bibliographic record

VenueEuropean Heart Journal · 2025
Typearticle
Languageen
FieldMedicine
TopicBlood Coagulation and Thrombosis Mechanisms
Canadian institutionsUniversity of WinnipegUniversity of Manitoba
Fundersnot available
KeywordsAMPKProtein kinase APhosphorylationMyocardial infarctionDownregulation and upregulationReceptorHypoxia (environmental)Contractility

Abstract

fetched live from OpenAlex

Abstract Background/Introduction Protease activated receptor 2 (PAR2) is a G protein-coupled receptor reported to regulate vascular contractility and heart failure. However, its role in mediating acute myocardial infarction is currently unclear. AMP-activated protein kinase (AMPK) is an enzyme that maintains cellular energy balance, and its activation during myocardial infarction plays a key role in preventing cardiomyocyte death and limiting post-ischemic cardiac damage. Purpose This study is the first to explore the relationship between PAR2 and AMPK in cardiomyocytes during ischemia, hoping to open up new therapeutic strategies for the treatment of post-ischemic cardiac injury. Methods In this study, we used PAR2 genetic knockout mice, Langendorff heart perfusion system and isolated primary adult cardiomyocytes, combined with molecular and cellular techniques, to investigate a novel signaling pathway by which PKA/CaMKKβ in regulating AMPK activity during hypoxia and ischemia. Results PAR2 is highly expressed in the heart. PAR2 deficiency significantly improved cardiac functional recovery and limited infarct size following acute global ischemia, which were associated with increased AMPK activation. Interestingly, knockdown of PAR2 in cardiomyocytes also improved AMPK and limited cell death following hypoxia, suggesting that cardiomyocyte PAR2 may be key to regulate cardiac ischemia-reperfusion injury. We also found that PAR2 activation stimulated PKA, leading to an inhibitory phosphorylation of the AMPK upstream kinase, CaMKKβ at Ser495. In addition, PAR2 activation promoted the binding of CaMKKβ to 14-3-3, a protein that maintains CaMKKβ inactivation. Thus, blocking PAR2 activation by GB83 upregulated AMPK by attenuating inhibitory phosphorylation of CaMKKβ and dissociating the binding between CaMKKβ and 14-3-3 during hypoxia. Conclusion Inhibition of cardiac PAR2 during acute ischemia can upregulate AMPK activity and cell survival through the PKA/CaMKKβ signaling pathway. Thus, the development of cardiac PAR2 as a pharmaceutical target will have important clinical significance for the future therapy of myocardial infarction.Graphic abstract

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 score0.004
Threshold uncertainty score0.013

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 communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0040.001

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 head0.031
GPT teacher head0.303
Teacher spread0.272 · 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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