Evidence map›Paper›PMID 40501383›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2025

Single-Cell Multimodal Profiling Reveals a Novel CD26

Alexander C Bashore, Johana Coronel, Chenyi Xue, Lucie Y Zhu, Muredach P Reilly

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In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. 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. Review
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  3. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors.

Alexander C BashoreCardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY (A.C.B.).ORCID 0000-0002-1380-9242
Johana CoronelDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (J.C., C.X., L.Y.Z., M.P.R.).ORCID 0000-0002-9257-0849
Chenyi XueDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (J.C., C.X., L.Y.Z., M.P.R.).ORCID 0000-0002-8829-7659
Lucie Y ZhuDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (J.C., C.X., L.Y.Z., M.P.R.).ORCID 0000-0002-1048-5377
Muredach P ReillyDivision of Cardiology, Department of Medicine, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY (J.C., C.X., L.Y.Z., M.P.R.).ORCID 0000-0002-3035-9386

Funding

Clinical and Translational Science AwardUL1TR001873 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI REILLY, MUREDACH P · 2016 to 2025
$99.0M
Smooth muscle cell-derived cell fates and cellular interactions in atherosclerotic plaque stability in disease progression and regression.R01HL166916 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Muredach P Reilly · 2023 to 2026
$2.8M
Identification of smooth muscle cell genes causal in atherosclerotic plaque stability and cardiovascular disease riskR01HL169766 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Muredach P Reilly, Danish Saleheen · 2023 to 2026
$2.6M
NCATS NIH HHS UL1 TR001873NHLBI NIH HHS R01 HL166916NHLBI NIH HHS R01 HL169766
6 · The paper itself

Abstract

backgroundAtherosclerosis involves complex interactions between lipids, immune cells, vascular smooth muscle cells, and fibroblasts within the arterial wall. While significant advances in single-cell technologies have shed light on the roles of immune cells and vascular smooth muscle cells in plaque development, fibroblasts remain underexplored, leaving critical gaps in understanding their contributions to disease progression and plaque stability. Comprehensive characterization of fibroblast phenotypes in atherosclerosis is essential to unravel their diverse functions and to distinguish between subsets that may play protective versus pathogenic roles in the disease process.

methodsHere, we utilized cellular indexing of transcriptomes and epitopes by sequencing to comprehensively profile fibroblast diversity in a mouse model of atherosclerosis. Mice were fed an atherogenic diet for 0, 8, 19, and 26 weeks, representing distinct stages of disease progression, enabling a detailed phenotypic characterization of fibroblasts throughout the course of atherosclerosis development.

resultsWe identified 4 distinct fibroblast subpopulations, including a myofibroblast population closely resembling vascular smooth muscle cell-derived chondromyocytes. The proportions of these fibroblast subsets exhibited a modest decline as atherosclerosis progressed. Through multimodal analysis, we identified CD26 (cluster of differentiation) as a highly expressed and specific marker for one of these fibroblast subpopulations, distinguishing it from other subsets. Using a combination of flow cytometry and immunohistochemistry, we demonstrated that CD26

conclusionsOur multiomic analysis highlights the phenotypic diversity and dynamic changes of fibroblasts during atherosclerosis progression. Among these, CD26

Indexed as

Aortic DiseasesAtherosclerosisDipeptidyl Peptidase 4FibroblastsSingle-Cell AnalysisAnimalsDisease Models, AnimalDisease ProgressionMaleMiceMice, Inbred C57BLMice, Knockout, ApoEPhenotypePlaque, AtheroscleroticTranscriptomeDipeptidyl Peptidase 4Dpp4 protein, mousearteriesatherosclerosisdisease progressionfibroblastsphenotype

Identifiers

PMID40501383
PMCPMC13274626

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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.