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Record W2582958156 · doi:10.1161/atvb.33.suppl_1.a79

Abstract 79: Examining the Role of Endoplasmic Reticulum Stress Induced Glycogen Synthase Kinase-3a/ß in Accelerated Atherosclerosis

2013· article· en· W2582958156 on OpenAlexaff
Cameron S. McAlpine, Geoff H. Werstuck

Bibliographic record

VenueArteriosclerosis Thrombosis and Vascular Biology · 2013
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicEndoplasmic Reticulum Stress and Disease
Canadian institutionsMcMaster University
Fundersnot available
KeywordsUnfolded protein responseEndoplasmic reticulumEndocrinologyInternal medicineGSK-3XBP1GSK3BTauroursodeoxycholic acidThapsigarginSteatosisGlycogen synthaseChemistryKinaseBiologyMedicineCell biologyGlycogenBiochemistry

Abstract

fetched live from OpenAlex

Introduction Cardiovascular disease accounts for a third of all deaths in the western world, however our understanding of the molecular mechanisms of atherosclerosis development is incomplete. Our previous findings have suggested that endoplasmic reticulum (ER) stress plays a causative role in atherogenesis. The objective of this study is to investigate how ER stress promotes atherosclerosis with a specific focus on ER stress-induced Glycogen Synthase Kinase (GSK)-3α and β. Methods and Results Established mouse models of accelerated atherosclerosis including hyperglycemia, hyperhomocysteinemia and relative dyslipidemia in female ApoE-/- mice were examined. A subset of mice from each group was supplemented with valproate (625 mg/kg), a compound with GSK3α/β inhibitory properties. Hyperglycemia, hyperhomocysteinemia and high fat diet elevated ER stress levels in multiple tissues, enhanced GSK3β activity, increased atherosclerotic plaque size, and induced hepatic steatosis. Valproate-supplementation significantly attenuated GSK3 activation, aortic plaque development and hepatic steatosis without altering ER stress levels. ER stress and valproate appears to modulate GSK3 activity by altering its phosphorylation status. To examine the mechanism linking ER stress to the activation of pro-atherogenic pathways, cultured THP1-derived macrophages were treated with the ER stress inducing agents, glucosamine (5mM), thapsigargin (1.5μM) or palmitate (800μM). GSK3α/β activity was inhibited with the specific inhibitor CT99021 (4μM). In macrophages, ER stress upregulated the mRNA expression of genes controlling lipid biosynthesis while GSK3α/β inhibition attenuated lipid synthesis. The expression of downstream targets of the PERK ER stress signaling pathway, CHOP and ATF4, were downregulated by GSK3α/β inhibition. Further, PERK-/- mouse embryonic fibroblasts (MEFs) had significantly attenuated lipid accumulation while expression of constitutively active GSK3β-S9A restored the ability of PERK deficient cells to accumulate lipids. Conclusions These findings support the a common pathway that links cardiovascular risk factors to the activationof pro-atherogenic pathways by a mechanism involving ER stress-induced GSK3α/β.

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 score0.006
Threshold uncertainty score0.019

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)0.0060.001

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 head0.028
GPT teacher head0.258
Teacher spread0.230 · 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
Published2013
Admission routes1
Has abstractyes

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