Evidence map›Paper›PMID 31019462›Full record

ReviewFrontiers in pharmacology2019

Macrophage Death as a Pharmacological Target in Atherosclerosis.

Wim Martinet, Isabelle Coornaert, Pauline Puylaert, Guido R Y De Meyer

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 2 pooled it
9.3field-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

123 citing papers in PubMed, 2 syntheses or guidelines pooled it, 209 citations in OpenAlex.

  1. Pooled it
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  3. Review
  4. Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026
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63 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.

Wim MartinetLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.
Isabelle CoornaertLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.
Pauline PuylaertLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.
Guido R Y De MeyerLaboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium.
University of Antwerp · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disorder characterized by the gradual build-up of plaques within the vessel wall of middle-sized and large arteries. Over the past decades, treatment of atherosclerosis mainly focused on lowering lipid levels, which can be accomplished by the use of statins. However, some patients do not respond sufficiently to statin therapy and therefore still have a residual cardiovascular risk. This issue highlights the need for novel therapeutic strategies. As macrophages are implicated in all stages of atherosclerotic lesion development, they represent an important alternative drug target. A variety of anti-inflammatory strategies have recently emerged to treat or prevent atherosclerosis. Here, we review the canonical mechanisms of macrophage death and their impact on atherogenesis and plaque stability. Macrophage death is a prominent feature of advanced plaques and is a major contributor to necrotic core formation and plaque destabilization. Mechanisms of macrophage death in atherosclerosis include apoptosis, passive or accidental necrosis as well as secondary necrosis, a type of death that typically occurs when apoptotic cells are insufficiently cleared by neighboring cells via a phagocytic process termed efferocytosis. In addition, less-well characterized types of regulated necrosis in macrophages such as necroptosis, pyroptosis, ferroptosis, and parthanatos may occur in advanced plaques and are also discussed. Autophagy in plaque macrophages is an important survival pathway that protects against cell death, yet massive stimulation of autophagy promotes another type of death, usually referred to as autosis. Multiple lines of evidence indicate that a better insight into the different mechanisms of macrophage death, and how they mutually interact, will provide novel pharmacological strategies to resolve atherosclerosis and stabilize vulnerable, rupture-prone plaques.

Indexed as

apoptosisatherosclerosisautophagycell deathferroptosismacrophagesnecroptosispyroptosis

Identifiers

PMID31019462
PMCPMC6458279
OpenAlexW2928482340

What OpenQuestion 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 OpenQuestion graph.