Evidence mapPaperPMID 33258000Full record

ReviewBasic research in cardiology2020

Mouse models of atherosclerosis and their suitability for the study of myocardial infarction.

Pelin Golforoush, Derek M Yellon, Sean M Davidson

Open access · hybridAbstract readReview
In one paragraph

Review in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
7.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. ILK-Dependent Modulation of DPP4 Prevents Progression of Calcific Aortic Valve Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  5. Article
  6. Monocyte Chemokines Enhance Atherosclerotic Plaque Necrosis After Bacterial Kidney Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
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  15. Review
  16. Article
  17. Molecular mechanisms and intervention approaches of heart failure (Review).International journal of molecular medicine · 2025
    Review
  18. Article
  19. Article
  20. Article

11 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Pelin GolforoushThe Hatter Cardiovascular Institute, 67 Chenies Mews, London, WC1E 6HX, UK.
Derek M YellonThe Hatter Cardiovascular Institute, 67 Chenies Mews, London, WC1E 6HX, UK.
Sean M DavidsonThe Hatter Cardiovascular Institute, 67 Chenies Mews, London, WC1E 6HX, UK. s.davidson@ucl.ac.uk.ORCID 0000-0001-5182-4980
UK Dementia Research Institute · GB

Funding

British Heart Foundation PG/19/51/34493
6 · The paper itself

Abstract

Atherosclerotic plaques impair vascular function and can lead to arterial obstruction and tissue ischaemia. Rupture of an atherosclerotic plaque within a coronary artery can result in an acute myocardial infarction, which is responsible for significant morbidity and mortality worldwide. Prompt reperfusion can salvage some of the ischaemic territory, but ischaemia and reperfusion (IR) still causes substantial injury and is, therefore, a therapeutic target for further infarct limitation. Numerous cardioprotective strategies have been identified that can limit IR injury in animal models, but none have yet been translated effectively to patients. This disconnect prompts an urgent re-examination of the experimental models used to study IR. Since coronary atherosclerosis is the most prevalent morbidity in this patient population, and impairs coronary vessel function, it is potentially a major confounder in cardioprotective studies. Surprisingly, most studies suggest that atherosclerosis does not have a major impact on cardioprotection in mouse models. However, a major limitation of atherosclerotic animal models is that the plaques usually manifest in the aorta and proximal great vessels, and rarely in the coronary vessels. In this review, we examine the commonly used mouse models of atherosclerosis and their effect on coronary artery function and infarct size. We conclude that none of the commonly used strains of mice are ideal for this purpose; however, more recently developed mouse models of atherosclerosis fulfil the requirement for coronary artery lesions, plaque rupture and lipoprotein patterns resembling the human profile, and may enable the identification of therapeutic interventions more applicable in the clinical setting.

Indexed as

Plaque, AtheroscleroticAnimalsAortic DiseasesAtherosclerosisCoronary Artery DiseaseDiet, High-FatDisease Models, AnimalGenetic Predisposition to DiseaseMice, Knockout, ApoEMyocardial InfarctionMyocardiumPhenotypeReceptors, LDLRupture, SpontaneousScavenger Receptors, Class BSpecies SpecificityReceptors, LDLScarb1 protein, mouseScavenger Receptors, Class BAtherosclerosisCardioprotectionCoronary arteryIschaemiaMiceMyocardial infarctionReperfusionVascular function

Identifiers

PMID33258000
PMCPMC7704510
OpenAlexW3108661591

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.