Evidence map›Paper›PMID 27493969›Full record

ReviewBioMed research international2016

Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis.

Yuri V Bobryshev, Ekaterina A Ivanova, Dimitry A Chistiakov, Nikita G Nikiforov, Alexander N Orekhov

Abstract readReview
In one paragraph

Review in BioMed research international, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed
–field-weighted citation impact
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

185 citing papers in PubMed.

  1. Article
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  10. Myeloperoxidase as a therapeutic target for oxidative damage in Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2025
    Review
  11. Article
  12. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  13. Review
  14. Article
  15. Article
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  18. Review
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125 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

5 authors.

Yuri V BobryshevInstitute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia; Faculty of Medicine, School of Medical Sciences, University of New South Wales, Kensington, Sydney, NSW 2052, Australia; School of Medicine, University of Western Sydney, Campbelltown, NSW 2560, Australia.ORCID 0000-0002-3745-321X
Ekaterina A IvanovaDepartment of Development and Regeneration, KU Leuven, 3000 Leuven, Belgium.ORCID 0000-0003-3159-2881
Dimitry A ChistiakovDepartment of Molecular Genetic Diagnostics and Cell Biology, Institute of Pediatrics, Research Center for Children's Health, Moscow 119991, Russia.
Nikita G NikiforovInstitute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia; Institute for Atherosclerosis, Skolkovo Innovation Center, Moscow 143025, Russia.
Alexander N OrekhovInstitute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow 125315, Russia; Institute for Atherosclerosis, Skolkovo Innovation Center, Moscow 143025, Russia; Department of Biophysics, Biological Faculty, Moscow State University, Moscow 119991, Russia.ORCID 0000-0002-6495-1628

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis can be regarded as a chronic inflammatory state, in which macrophages play different and important roles. Phagocytic proinflammatory cells populate growing atherosclerotic lesions, where they actively participate in cholesterol accumulation. Moreover, macrophages promote formation of complicated and unstable plaques by maintaining proinflammatory microenvironment. At the same time, anti-inflammatory macrophages contribute to tissue repair and remodelling and plaque stabilization. Macrophages therefore represent attractive targets for development of antiatherosclerotic therapy, which can aim to reduce monocyte recruitment to the lesion site, inhibit proinflammatory macrophages, or stimulate anti-inflammatory responses and cholesterol efflux. More studies are needed, however, to create a comprehensive classification of different macrophage phenotypes and to define their roles in the pathogenesis of atherosclerosis. In this review, we provide an overview of the current knowledge on macrophage diversity, activation, and plasticity in atherosclerosis and describe macrophage-based cellular tests for evaluation of potential antiatherosclerotic substances.

Indexed as

Models, ImmunologicalAnimalsAtherosclerosisCytokinesHumansInflammasomesMacrophage ActivationMacrophagesTranscriptomeCytokinesInflammasomes

Identifiers

PMID27493969
PMCPMC4967433

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.