Evidence map›Paper›PMID 41850847›Full record

ArticleJournal of atherosclerosis and thrombosis2026

A Single-Cell Analysis Reveals Macrophage Heterogeneity Driving Plaque Vulnerability in Coronary and Carotid Arteries.

Takeshi Yoshida, Takuo Emoto, Hiroyuki Yamamoto, Tomofumi Takaya, Takahiro Sawada, Sarah Louise Murphy, Mitsuhiko Shoda, Keisuke Nakamura, Masayuki Taniguchi, Naoto Sasaki and 8 more

Abstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–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

3 citing papers in PubMed.

  1. Article
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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

18 authors.

Takeshi YoshidaDivision of Advanced Medical and Pharmaceutical Sciences, Graduate School of Science, Technology and Innovation, Kobe University.
Takuo EmotoDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Hiroyuki YamamotoDivision of Cardiovascular Medicine, Department of Internal Medicine, Hyogo Prefectural Harima-Himeji General Medical Center.
Tomofumi TakayaDivision of Cardiovascular Medicine, Department of Internal Medicine, Hyogo Prefectural Harima-Himeji General Medical Center.
Takahiro SawadaDivision of Cardiovascular Medicine, Kakogawa Central City Hospital.
Sarah Louise MurphyDivision of Advanced Medical and Pharmaceutical Sciences, Graduate School of Science, Technology and Innovation, Kobe University.
Mitsuhiko ShodaDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Keisuke NakamuraDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Masayuki TaniguchiDivision of Pharmacology, Kobe University Graduate School of Medicine.
Naoto SasakiLaboratory of Medical Pharmaceutics, Kobe Pharmaceutical University.
Yuta FukuishiDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Takayoshi TobaDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Takenao OhkawaDepartment of Information and Intelligence Engineering, Kobe University.
Tomoyuki FuruyashikiDivision of Pharmacology, Kobe University Graduate School of Medicine.
Hiroya KawaiDivision of Community Medicine and Health Science, Kobe University Graduate School of Medicine.
Ken-Ichi HirataDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Hiromasa OtakeDivision of Cardiovascular Medicine, Department of Internal Medicine, Kobe University Graduate School of Medicine.
Tomoya YamashitaDivision of Advanced Medical and Pharmaceutical Sciences, Graduate School of Science, Technology and Innovation, Kobe University.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimAcute coronary syndrome (ACS) and ischemic stroke are major life-threatening conditions caused by atherosclerosis. Although the mechanisms of atherosclerosis appear to be broadly similar across different vascular beds, growing evidence suggests that there are morphological and histological differences between coronary and carotid atherosclerosis. To identify disease-specific therapeutic strategies, we aimed to compare ACS and chronic coronary syndrome (CCS) in coronary artery disease, and symptomatic and asymptomatic carotid artery disease.

methodsWe analyzed our own single-cell RNA sequencing dataset for coronary artery disease (GSE184073) and a publicly available dataset for carotid artery disease (GSE253903). Myeloid cells were extracted from these datasets and comparative analyses were performed using metabolic profiling and an RNA velocity analysis.

resultsBy integrating multiple velocity-inference approaches, including the original and dynamic RNA velocity models, TFvelo using transcription factor regulatory information, and CellRank, we consistently identified a differentiation trajectory toward interleukin-1B (IL1B)

conclusionsOur findings revealed a shared differentiation trajectory into IL1B

Indexed as

Acute Coronary SyndromeCarotid ArteriesCarotid Artery DiseasesCoronary Artery DiseaseCoronary VesselsMacrophagesPlaque, AtheroscleroticSingle-Cell AnalysisHumansAcute coronary syndromeCarotid artery diseaseCoronary artery diseaseIschemic strokeSingle-cell RNA sequencing

Identifiers

PMID41850847
PMCPMC13246284

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.