Evidence map›Paper›PMID 30830865›Full record

ArticleJCI insight2019

Single-cell analysis of fate-mapped macrophages reveals heterogeneity, including stem-like properties, during atherosclerosis progression and regression.

Jian-Da Lin, Hitoo Nishi, Jordan Poles, Xiang Niu, Caroline Mccauley, Karishma Rahman, Emily J Brown, Stephen T Yeung, Nikollaq Vozhilla, Ada Weinstock and 3 more

Abstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 199 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
199citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

199 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  20. Benzene metabolites increase vascular permeability by activating heat shock proteins and Rho GTPases.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article

139 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

13 authors.

Jian-Da LinDepartment of Microbiology and.
Hitoo NishiDepartment of Medicine, New York University School of Medicine, New York, New York, USA.
Jordan PolesDepartment of Microbiology and.
Xiang NiuTri-Institutional Program in Computational Biology and Medicine, Weill Cornell Medical College, New York, New York, USA.
Caroline MccauleyDepartment of Microbiology and.
Karishma RahmanDepartment of Medicine, New York University School of Medicine, New York, New York, USA.
Emily J BrownDepartment of Medicine, New York University School of Medicine, New York, New York, USA.
Stephen T YeungDepartment of Microbiology and.
Nikollaq VozhillaDepartment of Microbiology and.
Ada WeinstockDepartment of Medicine, New York University School of Medicine, New York, New York, USA.
Stephen A RamseyDepartment of Biomedical Sciences, School of Electrical Engineering and Computer Science, Oregon State University, Corvallis, Oregon, USA.
Edward A FisherDepartment of Microbiology and.
P'ng LokeDepartment of Microbiology and.

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Cheongeun Oh · 1985 to 2026
$83.1M
Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
Alternatively activated macrophages during helminth infectionR01AI133977 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI TORRES, VICTOR J. · 2017 to 2021
$2.4M
NCI NIH HHS P30 CA016087NHLBI NIH HHS R01 HL084312NIAID NIH HHS R01 AI133977
6 · The paper itself

Abstract

Atherosclerosis is a leading cause of death worldwide in industrialized countries. Disease progression and regression are associated with different activation states of macrophages derived from inflammatory monocytes entering the plaques. The features of monocyte-to-macrophage transition and the full spectrum of macrophage activation states during either plaque progression or regression, however, are incompletely established. Here, we use a combination of single-cell RNA sequencing and genetic fate mapping to profile, for the first time to our knowledge, plaque cells derived from CX3CR1+ precursors in mice during both progression and regression of atherosclerosis. The analyses revealed a spectrum of macrophage activation states with greater complexity than the traditional M1 and M2 polarization states, with progression associated with differentiation of CXC3R1+ monocytes into more distinct states than during regression. We also identified an unexpected cluster of proliferating monocytes with a stem cell-like signature, suggesting that monocytes may persist in a proliferating self-renewal state in inflamed tissue, rather than differentiating immediately into macrophages after entering the tissue.

Indexed as

AnimalsAtherosclerosisBone Marrow TransplantationCell DifferentiationCX3C Chemokine Receptor 1Diet, WesternDisease Models, AnimalDisease ProgressionHumansMacrophage ActivationMacrophagesMiceMice, KnockoutMonocyte-Macrophage Precursor CellsPlaque, AtheroscleroticReceptors, LDLCX3C Chemokine Receptor 1Cx3cr1 protein, mouseReceptors, LDLAtherosclerosisCardiologyImmunologyMacrophagesMolecular diagnosis

Identifiers

PMID30830865
PMCPMC6478411

What Socratic 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 Socratic graph.