Evidence map›Paper›PMID 42558046›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2026

Dual Lineage Tracing Identifies Cellular Mechanisms Underlying Radiation-Associated Changes in Atherosclerotic Lesion Composition-Brief Report.

Rebecca A Deaton, Tajbir Raihan, Victoria M Milosek, Fatema Allaham, Alexandra L Krinsky, Laura S Shankman, Alexander M Como, Gabriel F Alencar, Anita Salamon, Nazanin Moradinasab and 2 more

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Article in Arteriosclerosis, thrombosis, and vascular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Rebecca A DeatonRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0001-7569-1924
Tajbir RaihanRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0009-0009-9043-9968
Victoria M MilosekRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0003-3520-9931
Fatema AllahamCollege of Medicine, SUNY Downstate Health Sciences University, Brooklyn (F.A.).ORCID 0009-0001-3496-6765
Alexandra L KrinskyRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0009-0000-4099-8387
Laura S ShankmanRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0003-4983-9467
Alexander M ComoRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0009-0009-2012-3968
Gabriel F AlencarDepartment of Microbiology, Immunology and Cancer Biology (G.F.A.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0002-1752-7429
Anita SalamonRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0002-5708-9494
Nazanin MoradinasabSchool of Data Science, University of Virginia, Charlottesville (N.M.).ORCID 0000-0003-3881-8599
Subhashis BanerjeeRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0001-8971-0006
Gary K OwensRobert M. Berne Cardiovascular Research Center (R.A.D., T.R., V.M.M., A.L.K., L.S.S., A.M.C., A.S., S.B., G.K.O.), University of Virginia School of Medicine, Charlottesville.ORCID 0000-0002-7119-9657

Funding

Role of IL-6 trans signaling in atherosclerosis development and late-stage pathogenesisR01HL164367 · NHLBI · UNIVERSITY OF VIRGINIA · PI Gary K Owens · 2023 to 2026
$3.2M
Role of Smooth Muscle Cell Insulin Resistance and Systemic Metabolic Dysfunction in Atherosclerosis Development and Late Stage Lesion PathogenesisR01HL166161 · NHLBI · UNIVERSITY OF VIRGINIA · PI Gary K Owens · 2023 to 2026
$3.2M
Endothelial Cell to Mesenchymal Cell Transitions Play a Critical Biological Sex- and Aging-Dependent Role in Formation and Maintenance of the Acta2+ Atherosclerotic Lesion Protective Fibrous CapR01HL156849 · NHLBI · UNIVERSITY OF VIRGINIA · PI OWENS, GARY K · 2022 to 2025
$3.2M
Defining SMC phenotypes critical in late stage atherosclerosis pathogenesisR01HL136314 · NHLBI · UNIVERSITY OF VIRGINIA · PI OWENS, GARY K · 2018 to 2021
$3.0M
Role of Metabolic Reprogramming in Formation and Maintenance of the Acta2+ Atherosclerotic Lesion Protective Fibrous CapR01HL155165 · NHLBI · UNIVERSITY OF VIRGINIA · PI OWENS, GARY K · 2021 to 2024
$2.9M
NHLBI NIH HHS R01 HL136314NHLBI NIH HHS R01 HL155165NHLBI NIH HHS R01 HL156849NHLBI NIH HHS R01 HL164367NHLBI NIH HHS R01 HL166161
6 · The paper itself

Abstract

backgroundPhenotypic plasticity of smooth muscle cells (SMCs) and endothelial cells (ECs) contributes to atherosclerotic plaque composition and stability, yet how shifts in one population influence the contribution and function of the other under conditions of vascular stress, such as irradiation, is poorly understood. A major limitation has been the inability to simultaneously fate-map both cell types within the same lesion, with most studies mapping one lineage while inferring the other using unreliable dynamically changing marker genes, risking false-positive and false-negative assignment.

methodsWe generated dual lineage tracing

resultsDual lineage tracing simultaneously labeled SMC- and EC-derived cells in healthy and atherosclerotic vessels. Irradiation induced divergent responses: SMC-derived cells failed to invest in lesions and upregulated stress-activated inflammatory genes, whereas EC-derived cells expanded and upregulated SMC-associated genes. However, EC-derived cells within lesions failed to induce extracellular matrix genes, and lesions from irradiated mice exhibited reduced collagen content and fewer ACTA2 (α-smooth muscle actin)

conclusionsDual lineage tracing of SMCs and ECs demonstrated that irradiation-induced loss of lesional SMC and expansion of EC-derived ACTA2

Indexed as

AtherosclerosisCell LineageCell TrackingEndothelial CellsMuscle, Smooth, VascularMyocytes, Smooth MusclePlaque, AtheroscleroticActinsAnimalsCell PlasticityCells, CulturedDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, Knockout, ApoEActinsatherosclerosiscellular plasticityendothelial cellsextracellular matrixmyocytes, smooth muscleradiationrecombinases

Identifiers

PMID42558046
PMCPMC13449331

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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.