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Record W4404690229 · doi:10.26685/urncst.714

Contributions of Macrophages in the Disease Pathology of Myocardial Infarction and Atherosclerosis: A Literature Review

2024· review· en· W4404690229 on OpenAlexaff
Conrad Neil Canoneo

Bibliographic record

VenueUndergraduate Research in Natural and Clinical Science and Technology (URNCST) Journal · 2024
Typereview
Languageen
FieldMedicine
TopicCardiovascular Disease and Adiposity
Canadian institutionsUniversity of Toronto
Fundersnot available
KeywordsMyocardial infarctionMedicineProinflammatory cytokineInflammationMacrophageDiseaseInfarctionCoronary atherosclerosisInternal medicineCardiologyImmunologyMediatorCoronary artery diseaseBiologyIn vitro

Abstract

fetched live from OpenAlex

Introduction: Macrophages have been shown to play a role in the disease pathology of myocardial infarction and atherosclerosis, two prominent cardiovascular diseases. Understanding the mechanisms by which macrophages contribute to disease onset can serve as a valuable resource for the development of new therapeutics. This study specifically aims to identify the roles macrophages play in the regulation and progression of myocardial infarction and atherosclerosis in human and mice models, while highlighting current and developing treatments that target macrophages to prevent or delay these diseases. Methods: This review examines studies and previous reviews in the last 20 years that report proinflammatory mediators secreted by pro-inflammatory (M1-like) macrophages in humans and mice that are affected by myocardial infarction or atherosclerosis or have undergone simulated conditions. Discussion: Pro-inflammatory M1 macrophages influence both myocardial infarction and atherosclerosis via the secretion of proinflammatory mediators IL-1β, IL-1∝, IL-6, TNF-∝, VCAM-1, MMP-9, and MCP-1. These mediators are shown to promote adverse cardiac remodelling events in individuals with myocardial infarction including inflammation, increase in the infarcted area, and worsened left ventricular systolic function. For those with atherosclerosis, mediator release is correlated with lesion and plaque development due to increased leukocyte and lymphocyte migration. Mediators that directly influence either disease are also reported. As atherosclerosis is a risk factor for myocardial infarction, the overall promotion of atherosclerosis by both shared and specific inflammatory mediators therefore increases the likelihood an individual undergoes myocardial infarction. Current and developing treatments for myocardial infarction revolve around inhibiting mediator release and activity, whereas inducing macrophage polarization, inhibiting scavenger receptor activity, and inducing autophagy are the focus of therapeutic intervention for atherosclerosis. Conclusion: Proinflammatory macrophages show a prominent role in the pathogenesis of myocardial infarction and atherosclerosis, including the body’s ability to recover from these diseases. Further research should involve identifying macrophage phenotypes and improvements in drug delivery methods may serve as future avenues in improvement for macrophage-based medicines of common CVDs.

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)0.001
metaresearch head score (Gemma)0.002
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Not applicable · Consensus signal: none
GenreCandidate signal: Review · Consensus signal: Review
Teacher disagreement score0.006
Threshold uncertainty score0.011

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0010.002
Meta-epidemiology (narrow)0.0010.000
Meta-epidemiology (broad)0.0010.001
Bibliometrics0.0060.005
Science and technology studies0.0000.001
Scholarly communication0.0010.002
Open science0.0010.001
Research integrity0.0010.001
Insufficient payload (model declined to judge)0.0030.001

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 head0.052
GPT teacher head0.451
Teacher spread0.399 · 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 designNot applicable
Domainnot available
GenreReview

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
Published2024
Admission routes1
Has abstractyes

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