Evidence map›Paper›PMID 42206370›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2026

Liang Chen, Lu Lin, Zheyu Wang, Lu Yu, Bichen Ren, Siyuan Zhou, Penghui Wang, Yao Li, Eryi Lu, Zhihui Dong

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In one paragraph

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.

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

10 authors.

Liang Chen *Shanghai Institute of Infectious Disease and Biosecurity (L.C.), Fudan University, Shanghai, China.ORCID 0009-0007-5187-7936
Lu Lin *Department of Stomatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, China (L.L., E.L.).ORCID 0000-0002-9051-1415
Zheyu Wang *Shanghai Key Laboratory of Vascular Lesions and Remodeling, Department of Vascular Surgery, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, China (Z.W.).ORCID 0009-0007-4300-4262
Lu Yu *Department of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital (L.C., L.Y., B.R., P.W., Z.D.), Fudan University, Shanghai, China.
Bichen RenDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital (L.C., L.Y., B.R., P.W., Z.D.), Fudan University, Shanghai, China.ORCID 0000-0002-6021-0208
Siyuan ZhouDepartment of Vascular Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, China (S.Z.).ORCID 0009-0003-4353-8740
Penghui WangDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital (L.C., L.Y., B.R., P.W., Z.D.), Fudan University, Shanghai, China.ORCID 0000-0002-7356-8401
Yao LiCenter for Vascular Surgery and Wound Care, Jinshan Hospital (Y.L., Z.D.), Fudan University, Shanghai, China.ORCID 0009-0000-6542-5585
Eryi LuDepartment of Stomatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, China (L.L., E.L.).ORCID 0000-0002-0045-2571
Zhihui DongDepartment of Vascular Surgery, Institute of Vascular Surgery, Zhongshan Hospital (L.C., L.Y., B.R., P.W., Z.D.), Fudan University, Shanghai, China.ORCID 0000-0002-3754-2458

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBacterial communities and their metabolites are increasingly recognized as key contributors to cardiovascular disease, yet their role and mechanistic involvement in abdominal aortic aneurysm (AAA) pathogenesis remain insufficiently defined.

methodsDental plaques from patients with AAA and matched healthy controls were subjected to metagenomic sequencing, and corresponding plasma samples underwent untargeted metabolomic profiling. In vivo, mice were topically exposed in the oral cavity to

resultsPatients with AAA showed a marked enrichment of Fn in dental plaque, and topical application of Fn aggravated AngII-induced AAA in mice. Elevated plasma isoleucine concentrations were observed in both human AAA and experimental models. Genetic deletion of

conclusionsFn-derived isoleucine drives ferroptosis in smooth muscle cells via H3K9ac-mediated activation of ACSL4, delineating a microbiota-metabolite-epigenetic axis in AAA pathogenesis and nominating dental plaque Fn abundance and circulating isoleucine as exploratory biomarker candidates requiring larger, independent validation.

Indexed as

Aortic Aneurysm, AbdominalFerroptosisFusobacterium nucleatumIsoleucineMuscle, Smooth, VascularMyocytes, Smooth MuscleAngiotensin IIAnimalsCase-Control StudiesDisease Models, AnimalDisease ProgressionFemaleHumansMaleMiceMice, Inbred C57BLAngiotensin IIIsoleucineaortic aneurysm, abdominalferroptosisFusobacterium nucleatumisoleucinemyocytes, smooth muscle

Identifiers

PMID42206370
PMCPMC13384373

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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.