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Therapeutic inhibition of RIP1 improves metabolic dysfunction and inhibits atherosclerosis in mouse models of cardiometabolic diseases

2018· article· en· W3177066123 on OpenAlexaff
Denuja Karunakaran, My Anh Nguyen, Michèle Geoffrion, Zachary Lister, Joshua W. Kandiah, Hailey Wyatt, Ana Mompeón, Ella deKemp, Richard Lee, Katey J. Rayner

Bibliographic record

VenueThe FASEB Journal · 2018
Typearticle
Languageen
FieldImmunology and Microbiology
TopicBiomarkers in Disease Mechanisms
Canadian institutionsUniversity of Ottawa
Fundersnot available
KeywordsNecroptosisInflammationMedicineEndocrinologyInsulin resistanceInternal medicineGene knockdownApoptosisProinflammatory cytokineMacrophage polarizationSOCS3ImmunologyInsulinProgrammed cell deathMacrophageChemistryIn vitroBiochemistryCancer

Abstract

fetched live from OpenAlex

Introduction Chronic activation of the innate immune system drives inflammation and contributes directly to obesity, insulin resistance and atherosclerosis. Previously we showed that necroptosis, a pro‐inflammatory form of programmed cell death, is activated in the vessel wall and drives atherosclerosis via activation of RIP3 and MLKL. We sought to determine upstream genetic regulators of necroptosis in atherosclerosis and metabolic disease, and hypothesized that gene expression of RIP1, a key regulatory kinase upstream of NFkB activation, apoptosis and necroptosis, drives macrophage inflammation in cardiometabolic diseases. Methods RIP1 anti‐sense oligonucleotides (ASOs, 2 unique sequences) were used to reduce RIP1 expression in 2 mouse models: i) atherosclerotic model [ApoE −/− mice fed a western diet for 8wks] and ii) diet‐induced obesity (DIO) model [C57Bl/6 male mice fed a high fat diet for 24 wks]. Mice were given weekly injections of RIP1 ASOs (50 or 100mg/kg) or control ASO (non‐targeting). Results RIP1 ASO treated ApoE −/− mice had a marked reduction in aortic sinus and en face lesion areas (47.2% or 58.8% decrease relative to control, p<0.01) and plasma inflammatory cytokines (IL‐1a, IL‐17A, p<0.05). RIP1 knockdown in macrophages decreased inflammatory gene expression (NFkB, TNFa, IL‐1a) and in vivo LPS‐induced NFkB activation. In obese mice, RIP1 ASOs strikingly decreased body weight (25% decrease versus control p<0.001) and total fat mass (50–65% decrease versus control, p<0.001). Further, insulin resistance was improved in RIP1 ASO treated mice (fasted blood glucose: 10.9mM in control versus 8.5±mM in RIP1 ASO, p<0.001; GTT and ITT both p<0.001). In humans, we identified 5 novel SNPs in strong linkage disequilibrium in or nearby RIP1 gene exon 5. Notably, in a cohort of >1,800 people, individuals carrying the minor allele of these RIP1 SNPs have a 75–89% increase in the risk of developing obesity (adjusted odds ratios: 1.75–1.89, p<10 −5 ) and a significant increase in RIP1 mRNA expression in adipose tissue (eQTL association in METSIM cohort, p=10 −23 ). Conclusions : We have identified RIP1 as central a driver of insulin resistance, obesity, and atherosclerosis and demonstrate the potential of RIP1 as a novel therapeutic target. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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)0.001
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: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.022
Threshold uncertainty score0.428

Codex and Gemma teacher scores by category

CategoryCodexGemma
Metaresearch0.0010.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.001
Scholarly communication0.0000.000
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 head0.017
GPT teacher head0.223
Teacher spread0.206 · 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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Citations1
Published2018
Admission routes1
Has abstractyes

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