Evidence map›Paper›PMID 42232307›Full record

ArticleFrontiers in cardiovascular medicine2026

NMN protects vascular endothelial cells from M1 macrophage-derived IL-1β-induced hyperpermeability by inhibiting VE-cadherin degradation.

Takeshi Katayoshi, Takahisa Nakajo, Natsuko Kitajima, Wakana Naka, Yuki Kamei, Taiki Fushimi, Masakatsu Kageyama, Mitsugu Akagawa, Kentaro Tsuji

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Article in Frontiers in cardiovascular medicine, 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

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

9 authors.

Takeshi KatayoshiDHC Corporation Laboratories, Division 2, Chiba, Japan.
Takahisa NakajoDHC Corporation Laboratories, Division 2, Chiba, Japan.
Natsuko KitajimaDHC Corporation Laboratories, Division 2, Chiba, Japan.
Wakana NakaDHC Corporation Laboratories, Division 2, Chiba, Japan.
Yuki KameiDepartment of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Taiki FushimiDepartment of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Masakatsu KageyamaDHC Corporation Laboratories, Division 2, Chiba, Japan.
Mitsugu AkagawaDepartment of Food Science, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima, Japan.
Kentaro TsujiDHC Corporation Laboratories, Division 2, Chiba, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and aims: Vascular endothelial (VE) dysfunction, particularly endothelial hyperpermeability, is a critical pathological process in various inflammatory vascular diseases, including atherosclerosis, vasculitis, and sepsis. Nicotinamide mononucleotide (NMN), an NAD Methods: A three-dimensional co-culture model of human umbilical vein endothelial cells (HUVECs) and M1 macrophages was constructed to reproduce inflammatory vascular microenvironments. Endothelial permeability was evaluated by measuring fluorescently labelled dextran and LDL passages from the luminal (top) to the abluminal side (bottom) of the insert. Results: M1 macrophage co-culture increased HUVEC permeability, and NMN pretreatment attenuated this hyperpermeability. Mechanistic analysis revealed that interleukin-1β (IL-1β) released by M1 macrophages was the primary contributor to endothelial hyperpermeability. NMN suppressed IL-1β-induced cell-cell gap formation and VE-cadherin degradation in HUVECs by inhibiting nuclear factor kappa B (NF- Conclusions: This

Indexed as

hyperpermeabilityinterleukin-1β (IL-1β)m1 macrophagesNMN (Nicotinamide mononucleotide)vascular endothelial cellsVE-cadherin degradation

Identifiers

PMID42232307
PMCPMC13222840

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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.