Evidence map›Paper›PMID 41526223›Full record

ArticleJournal of atherosclerosis and thrombosis2026

The Blockade of Delta-Like Ligand 1 Inhibits Atherosclerotic Lesion Formation and Attenuates Plaque Vulnerability.

Nasanbadrakh Orkhonselenge, Jun-Ichiro Koga, Daiki Kakumori, Yuki Kondo, Keisuke Hidaka, Tomohiro Shirouzu, Hiromichi Ueno, Hideo Yagita, Yosuke Nishimura, Masaharu Kataoka

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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 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Article
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

10 authors.

Nasanbadrakh OrkhonselengeThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Jun-Ichiro KogaThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Daiki KakumoriThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Yuki KondoThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Keisuke HidakaThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Tomohiro ShirouzuThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Hiromichi UenoThe Second Department of Internal Medicine, University of Occupational and Environmental Health.
Hideo YagitaThe Department of Immunology, Juntendo University.
Yosuke NishimuraThe Department of Cardiovascular Surgery, University of Occupational and Environmental Health.
Masaharu KataokaThe Second Department of Internal Medicine, University of Occupational and Environmental Health.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimNotch signaling is a fundamental signal that regulates morphogenesis and cell differentiation during the embryonic period, and it plays a crucial role in macrophage differentiation. Macrophage-mediated inflammation promotes atherosclerosis from the initial lesion formation to acute thrombotic complications in advanced plaques. However, their role in atherosclerosis remains unclear. We herein focused on the Notch ligand Delta-like ligand 1 (Dll1), and examined its role in the pathobiology of atherosclerosis.

methodsIn Apoe

resultsDll1 blockade suppressed both initial lesion development and plaque vulnerability compared with lesions in mice treated with non-immune IgG. Dll1 Ab decreased lipid accumulation in advanced lesions and increased the collagen content. In ex vivo cultured macrophages, the blockade of Dll1-Notch signaling by Dll1 blocking antibodies suppressed the mRNA expression of Tnf and the release of activated matrix metalloproteinase 9, which increased plaque vulnerability. In contrast, the stimulation of Dll1-Notch by recombinant Dll1 induced Il1b, Il6, and Tnf expression in macrophages, as well as NF-κB activation. An exploratory transcriptome analysis of atherosclerotic arteries suggested that Dll1-Notch signaling regulates the expression of genes associated with inflammation and mitosis.

conclusionsThese results indicate that Dll1 promotes the pathobiology of atherosclerosis from the initial lesion development to plaque destabilization in advanced atherosclerotic lesions.

Indexed as

AtherosclerosisCalcium-Binding ProteinsIntercellular Signaling Peptides and ProteinsMembrane ProteinsPlaque, AtheroscleroticAnimalsApolipoproteins EMacrophagesMaleMiceReceptors, NotchSignal TransductionApolipoproteins ECalcium-Binding ProteinsDlk1 protein, mouseIntercellular Signaling Peptides and ProteinsMembrane ProteinsReceptors, NotchAtherosclerosisMacrophagesNotch signalPlaque vulnerability

Identifiers

PMID41526223
PMCPMC13246286

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.