Evidence map›Paper›PMID 26892964›Full record

ReviewCirculation research2016

Macrophage Phenotype and Function in Different Stages of Atherosclerosis.

Ira Tabas, Karin E Bornfeldt

Open access · greenAbstract readReview
In one paragraph

Review in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 621 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
621citing papers in PubMed, 4 pooled it
41.2field-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

621 citing papers in PubMed, 4 syntheses or guidelines pooled it, 1,080 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Ilexoside K Ameliorates Atherosclerosis by Suppressing CD72Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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561 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.

Ira TabasFrom the Departments of Medicine (I.T.), Anatomy and Cell Biology (I.T.), and Physiology and Cellular Biophysics (I.T.), Columbia University, New York; and the Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition (K.E.B.) and Department of Pathology (K.E.B.), UW Diabetes Institute, University of Washington School of Medicine, Seattle.
Karin E BornfeldtFrom the Departments of Medicine (I.T.), Anatomy and Cell Biology (I.T.), and Physiology and Cellular Biophysics (I.T.), Columbia University, New York; and the Department of Medicine, Division of Metabolism, Endocrinology, and Nutrition (K.E.B.) and Department of Pathology (K.E.B.), UW Diabetes Institute, University of Washington School of Medicine, Seattle. bornf@u.washington.edu.
Columbia University · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Julie Mathieu · 1986 to 2026
$41.4M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI HEINECKE, JAY W · 2008 to 2019
$23.5M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
HYPERGLYCEMIA, PROTEIN KINASES AND SMOOTH MUSCLE GROWTHR01HL062887 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 1998 to 2014
$4.7M
Obesity and Arterial MetabolismR01HL126028 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2015 to 2018
$1.7M
APOC3, HDL Function and Cardiovascular Complications of T1DMDP3DK108209 · NIDDK · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E., HEINECKE, JAY W · 2015 to 2015
$1.6M
Mechanisms of Defective Efferocytosis in AtherosclerosisR01HL107497 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2012 to 2015
$1.6M
NHLBI NIH HHS HHSN268201000045CNHLBI NIH HHS P01 HL092969NHLBI NIH HHS P01HL092969NHLBI NIH HHS R01 HL062887NHLBI NIH HHS R01HL062887NHLBI NIH HHS R01 HL075662NHLBI NIH HHS R01 HL107497NHLBI NIH HHS R01HL107497NHLBI NIH HHS R01 HL126028NHLBI NIH HHS R01HL126028NIDDK NIH HHS DP3 DK108209NIDDK NIH HHS DP3DK108209NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30DK017047PHS HHS HHSN268201000045C
6 · The paper itself

Abstract

The remarkable plasticity and plethora of biological functions performed by macrophages have enticed scientists to study these cells in relation to atherosclerosis for >50 years, and major discoveries continue to be made today. It is now understood that macrophages play important roles in all stages of atherosclerosis, from initiation of lesions and lesion expansion, to necrosis leading to rupture and the clinical manifestations of atherosclerosis, to resolution and regression of atherosclerotic lesions. Lesional macrophages are derived primarily from blood monocytes, although recent research has shown that lesional macrophage-like cells can also be derived from smooth muscle cells. Lesional macrophages take on different phenotypes depending on their environment and which intracellular signaling pathways are activated. Rather than a few distinct populations of macrophages, the phenotype of the lesional macrophage is more complex and likely changes during the different phases of atherosclerosis and with the extent of lipid and cholesterol loading, activation by a plethora of receptors, and metabolic state of the cells. These different phenotypes allow the macrophage to engulf lipids, dead cells, and other substances perceived as danger signals; efflux cholesterol to high-density lipoprotein; proliferate and migrate; undergo apoptosis and death; and secrete a large number of inflammatory and proresolving molecules. This review article, part of the Compendium on Atherosclerosis, discusses recent advances in our understanding of lesional macrophage phenotype and function in different stages of atherosclerosis. With the increasing understanding of the roles of lesional macrophages, new research areas and treatment strategies are beginning to emerge.

Indexed as

AnimalsArteriesAtherosclerosisCell DifferentiationCellular MicroenvironmentCholesterolFoam CellsHumansInflammation MediatorsMacrophagesPhenotypePlaque, AtheroscleroticSignal TransductionCholesterolInflammation Mediatorsatherosclerosischolesterolfoam cellsmacrophagephenotype

Identifiers

PMID26892964
PMCPMC4762068
OpenAlexW2276012049

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.