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Targeting macrophage necroptosis for therapeutic and diagnostic interventions to treat atherosclerosis

2016· article· en· W2559953260 on OpenAlexaff
Denuja Karunakaran, Michèle Geoffrion, Lihui Wei, Wei Gan, Ljubica Perisic, Lars Mäegdefessel, Ulf Hedin, Subash Sad, Renu Virmani, Terrence D. Ruddy, Katey J. Rayner

Bibliographic record

VenueThe FASEB Journal · 2016
Typearticle
Languageen
FieldImmunology and Microbiology
TopicPhagocytosis and Immune Regulation
Canadian institutionsOttawa Heart Institute
Fundersnot available
KeywordsNecroptosisProgrammed cell deathInflammationApoptosisCancer researchLesionMacrophageNecrosisCell biologyPathogenesisTumor necrosis factor alphaBiologyImmunologyPathologyMedicineIn vitroBiochemistry

Abstract

fetched live from OpenAlex

Atherosclerosis is a disease of maladaptive inflammation driven primarily by macrophages, and as the atherosclerotic plaque progresses and becomes more complex, a necrotic core forms that ultimately underlies the instability that drives plaque rupture and myocardial infarction. Necroptosis or ‘programmed necrosis’ is an emerging cell death pathway involving kinases RIP3 and MLKL that in contrast to apoptosis, induces a pro‐inflammatory state. We hypothesize that macrophages undergo necroptosis in response to atherogenic stimuli in the vessel wall, and this process underlies necrotic core formation and plaque instability. Here, we show that oxidized LDL (oxLDL) induces necroptotic cell death in macrophages, which can be blocked by Nec‐1, a necroptosis inhibitor. Macrophages treated with oxidized LDL have increased expression of necroptotic genes RIP3 and MLKL through activation of the promoter region and increased RIP3 and MLKL phosphorylation‐ critical steps in the execution of necroptosis. Further, the combined treatment with oxLDL and DAMPs (damage associated molecular patterns) amplified macrophage necroptotic cell death, indicating that additional inflammatory stimuli present in the lesion could act synergistically to promote necroptosis. In a model of established atherosclerosis, Nec‐1 intervention in Apoe −/− mice reduced lesion size (p<0.05) and markers of plaque instability, including reduced necrotic core formation (62.6% reduction, p<0.01). Further, we developed a novel 123 I‐Nec‐1 radiotracer targeting the necroptosis pathway and show that it specifically localizes to and tightly correlates with atherosclerotic lesions. Lastly, in humans with unstable carotid atherosclerosis, expression of the necroptotic genes RIP3 and MLKL is elevated and MLKL phosphorylation is detected in advanced atheromas, indicating that the necroptotic pathway is highly activated in vulnerable plaques. In conclusion , our findings offer molecular insight into the mechanisms by which inflammatory atherogenic ligands drives cell death necrotic core formation that underlies unstable atherosclerosis and identify innovative diagnostic and therapeutic tools to treat atherosclerosis.

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: none
Teacher disagreement score0.002
Threshold uncertainty score0.006

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0010.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0010.000
Open science0.0000.000
Research integrity0.0010.002
Insufficient payload (model declined to judge)0.0020.001

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 head0.030
GPT teacher head0.273
Teacher spread0.243 · 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
Published2016
Admission routes1
Has abstractyes

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