Evidence map›Paper›PMID 21841486›Full record

ReviewCurrent opinion in lipidology2011

Phenotypic modulation of macrophages in response to plaque lipids.

Samantha Adamson, Norbert Leitinger

Abstract readReview
In one paragraph

Review in Current opinion in lipidology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

73 citing papers in PubMed, 149 citations in OpenAlex.

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  12. Reversal of atherosclerosis by restoration of vascular copper homeostasis.Experimental biology and medicine (Maywood, N.J.) · 2024
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13 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

2 authors at 1 institution in 1 country.

Samantha AdamsonDepartment of Pharmacology, University of Virginia, Charlottesville, Virginia 22908, USA.
Norbert Leitinger
University of Virginia · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007267 · NIGMS · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI GARCIA-BLANCO, MARIANO A. · 1985 to 2024
$13.4M
Oxidized Phospholipid-Induced Inflammation in AtherosclerosisR01HL084422 · NHLBI · UNIVERSITY OF VIRGINIA · PI LEITINGER, NORBERT · 2006 to 2010
$1.7M
NHLBI NIH HHS R01 HL084422NHLBI NIH HHS R01-HL-084422
6 · The paper itself

Abstract

purpose of reviewThe accumulation of macrophages in the vascular wall is a hallmark of atherosclerosis. The biological properties of atherosclerotic plaque macrophages determine lesion size, composition, and stability. In atherosclerotic plaques, macrophages encounter a microenvironment that comprises a variety of lipid oxidation products, each of which has diverse biological effects. In this review, we summarize recent advances in our understanding of the effects of plaque lipids on macrophage phenotypic polarization. RECENT

findingsAtherosclerotic lesions in mice and in humans contain various macrophage phenotypes, which play different roles in mediating inflammation, the clearance of dead cells, and possibly resolution. Macrophages alter their phenotype and biological function in response to plaque lipids through the upregulation of specific sets of genes. Interaction of oxidized lipids with pattern recognition receptors and activation of the inflammasome by cholesterol crystals drive macrophages toward an inflammatory M1 phenotype. A new phenotype, Mox, develops when oxidized phospholipids activate stress response genes via Nrf2. Other lipid mediators such as nitrosylated-fatty acids and omega-3 fatty acid-derived products polarize plaque macrophages toward anti-inflammatory and proresolving phenotypes. SUMMARY: A deeper understanding of how lipids that accumulate in atherosclerotic plaques affect macrophage phenotype and function and thus atherosclerotic lesion development and stability will help to devise novel strategies for intervention.

Indexed as

AnimalsAtherosclerosisHumansInflammationLipid MetabolismMacrophagesOxidation-Reduction

Identifiers

PMID21841486
PMCPMC3979355
OpenAlexW2011947002

What OpenQuestion holds

Textmetadata
LicenceTDM
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.