Evidence map›Paper›PMID 24855200›Full record

ReviewCirculation research2014

Mechanisms that regulate macrophage burden in atherosclerosis.

Gwendalyn J Randolph

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed
12.4field-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, 259 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. The role of immune cells in different stages of atherosclerosis.International journal of medical sciences · 2024
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  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

1 author at 1 institution in 1 country.

Gwendalyn J RandolphFrom the Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO. grandolph@path.wustl.edu.
Washington University in St. Louis · US

Funding

Differentiation/migratory fate of monocyte-derived cellsR01AI049653 · NIAID · WASHINGTON UNIVERSITY · PI Gwendalyn J Randolph · 2000 to 2026
$4.6M
Pathways that regulate monocyte/dendritic cell migrationR01AI061741 · NIAID · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2007 to 2011
$2.0M
VEGF-C/VEGFR3 AND LYMPHATIC TRANSPORT OF CHOLESTEROL FROM ATHEROSCLEROTIC PLAQUER01HL118206 · NHLBI · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J · 2014 to 2017
$1.5M
Cholesterol and Lymphatic Transport of Molecules and CellsR01HL096539 · NHLBI · WASHINGTON UNIVERSITY · PI RANDOLPH, GWENDALYN J, SWARTZ, MELODY ANN · 2009 to 2012
$1.5M
NHLBI NIH HHS HL096539NHLBI NIH HHS R01 HL096539NHLBI NIH HHS R01 HL118206NIAID NIH HHS R01 AI049653NIAID NIH HHS R01 AI061741
6 · The paper itself

Abstract

Mononuclear phagocytes (MPs) relevant to atherosclerosis include monocytes, macrophages, and dendritic cells. A decade ago, studies on macrophage behavior in atherosclerotic lesions were often limited to quantification of total macrophage area in cross-sections of plaques. Although technological advances are still needed to examine plaque MP populations in an increasingly dynamic and informative manner, innovative methods to interrogate the biology of MPs in atherosclerotic plaques developed in the past few years point to several mechanisms that regulate the accumulation and function of MPs within plaques. Here, I review the evolution of atherosclerotic plaques with respect to changes in the MP compartment from the initiation of plaque to its progression and regression, discussing the roles that recruitment, proliferation, and retention of MPs play at these different disease stages. Additional work in the future will be needed to better distinguish macrophages and dendritic cells in plaque and to address some basic unknowns in the field, including just how cholesterol drives accumulation of macrophages in lesions to build plaques in the first place and how macrophages as major effectors of innate immunity work together with components of the adaptive immune response to drive atherosclerosis. Answers to these questions are sought with the goal in mind of reversing disease where it exists and preventing its development where it does not.

Indexed as

AnimalsAtherosclerosisCell ProliferationDendritic CellsDisease Models, AnimalDisease ProgressionFoam CellsHumansImmunity, InnateMacrophagesMicePlaque, Atheroscleroticatherosclerosismacrophagesmonocytes

Identifiers

PMID24855200
PMCPMC4059102
OpenAlexW2150350943

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.