Evidence map›Paper›PMID 41648299›Full record

ArticlebioRxiv : the preprint server for biology2026

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

Rebecca A Deaton, Tajbir Raihan, Victoria M Milosek, Fatema Allaham, Alexandra L Krinsky, Laura S Shankman, Gabriel F Alencar, Anita Salamon, Nazanin Moradinasab, Subhashis Banerjee and 1 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for 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.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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

11 authors.

Victoria M MilosekORCID 0000-0003-3520-9931
Fatema Allaham
Alexandra L Krinsky
Gabriel F AlencarORCID 0000-0002-1752-7429
Nazanin MoradinasabORCID 0000-0003-3881-8599
Subhashis BanerjeeORCID 0000-0001-8971-0006

Funding

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
NHLBI NIH HHS R01 HL156849NHLBI NIH HHS R01 HL166161
6 · The paper itself

Abstract

Background: Phenotypic 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 Methods: We generated dual lineage-tracing Results: Dual lineage tracing specifically and 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 Conclusions: Dual lineage-tracing of SMCs and ECs demonstrated that irradiation-induced loss of lesional SMC and expansion of EC-derived ACTA2 Clinical Perspective:

Identifiers

PMID41648299
PMCPMC12871099

What OpenQuestion holds

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Registered trials

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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.