Evidence map›Paper›PMID 38163815›Full record

ReviewNature reviews. Cardiology2024

Programmed death of macrophages in atherosclerosis: mechanisms and therapeutic targets.

Guido R Y De Meyer, Michelle Zurek, Pauline Puylaert, Wim Martinet

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 1 pooled it
36.5field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 1 synthesis or guideline pooled it, 156 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  5. Article
  6. Theaflavin attenuates atherosclerosis by targeting GSK-3β to suppress pyroptosis and Promote Autophagy in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  7. Article
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  9. Article
  10. Review
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  15. MLK3 promotes atherosclerosis by regulating ferroptosis in macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. Article

68 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

4 authors at 1 institution in 1 country.

Guido R Y De MeyerLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium. guido.demeyer@uantwerpen.be.ORCID 0000-0003-3848-8702
Michelle ZurekLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.ORCID 0000-0003-0564-1168
Pauline PuylaertLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.ORCID 0000-0002-0316-2916
Wim MartinetLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.ORCID 0000-0003-1967-9343
University of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a progressive inflammatory disorder of the arterial vessel wall characterized by substantial infiltration of macrophages, which exert both favourable and detrimental functions. Early in atherogenesis, macrophages can clear cytotoxic lipoproteins and dead cells, preventing cytotoxicity. Efferocytosis - the efficient clearance of dead cells by macrophages - is crucial for preventing secondary necrosis and stimulating the release of anti-inflammatory cytokines. In addition, macrophages can promote tissue repair and proliferation of vascular smooth muscle cells, thereby increasing plaque stability. However, advanced atherosclerotic plaques contain large numbers of pro-inflammatory macrophages that secrete matrix-degrading enzymes, induce death in surrounding cells and contribute to plaque destabilization and rupture. Importantly, macrophages in the plaque can undergo apoptosis and several forms of regulated necrosis, including necroptosis, pyroptosis and ferroptosis. Regulated necrosis has an important role in the formation and expansion of the necrotic core during plaque progression, and several triggers for necrosis are present within atherosclerotic plaques. This Review focuses on the various forms of programmed macrophage death in atherosclerosis and the pharmacological interventions that target them as a potential means of stabilizing vulnerable plaques and improving the efficacy of currently available anti-atherosclerotic therapies.

Indexed as

AtherosclerosisPlaque, AtheroscleroticApoptosisHumansMacrophagesNecrosis

Identifiers

PMID38163815
OpenAlexW4390507681

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.