Evidence map›Paper›PMID 41053533›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

FMO2 Promotes Angiogenesis via Regulation of N-Acetylornithine.

Jingyi Wang, Yinghui Xu, Xianpeng Wu, Mo Li, Changchen Xiao, Zaiyang Fu, Yongjian Chen, Qingju Li, Yating Ruan, Jing Zhao and 6 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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. Article
  2. FMO2 Promotes Angiogenesis via Regulation of N-Acetylornithine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    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

16 authors.

Jingyi WangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Yinghui XuDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Xianpeng WuDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Mo LiDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Changchen XiaoDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Zaiyang FuDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Yongjian ChenDepartment of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, China.
Qingju LiDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Yating RuanDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Jing ZhaoDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Zhiwei ZhongDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Jinghai ChenDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Wei ZhuDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Jinliang NanDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Cheng NiDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.
Xinyang HuDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China.ORCID https://orcid.org/0000-0002-6699-8470

Funding

Binjiang Institute of Zhejiang University ZY202205SMKY001Binjiang Institute of Zhejiang University ZY202205SMKY002Central Guidance on Local Science and Technology Development Fund of Zhejiang Province 2024ZY01044Fundamental Research Funds for the Central Universities 226-2023-00156Key R&D projects of Zhejiang Province 2021C03097Key R&D projects of Zhejiang Province 2023C03086National Key R&D Program of China 2023YFA1800700National Key R&D Program of China 2023YFA1800704National Key R&D Program of China 2024YFC3044500National Natural Science Foundation of China 82030014National Natural Science Foundation of China 82070253National Natural Science Foundation of China 82200275National Natural Science Foundation of China 82225004National Natural Science Foundation of China 82370240National Natural Science Foundation of China 82430013Transvascular Implantation Devices Research Institute KY012025002
6 · The paper itself

Abstract

Endothelial cell (EC) metabolism is an emerging target for proangiogenic treatment of ischemic diseases; however, little is known about the metabolic alterations in ECs during ischemic diseases or vessel development stages. By conducting single-cell transcriptome analysis, this work identifies flavin-containing monooxygenase 2 (FMO2) as a pivotal regulator under multiple ischemic conditions. Targeted EC compensation of FMO2 in the genetic ablation model proved its proangiogenic function in various ischemic models and in the developing retina. Metabolomics combined with EC single-cell sequencing revealed N-acetylornithine as the top-ranked altered metabolite regulated by FMO2, which inactivates NOTCH1 expression through the transcriptome regulation of activating transcription factor 3 (ATF3). N-acetylornithine delivery displays a proangiogenic therapeutic effect in the ischemic models. The therapeutic effects of FMO2 and N-acetylornithine can also be recapitulated in human ECs. These findings provide insights into the proangiogenic mechanisms underlying FMO2 and N-acetylornithine, revealing potential targets to treat ischemic disease.

Indexed as

IschemiaNeovascularization, PhysiologicOrnithineOxygenasesAngiogenesisAnimalsDisease Models, AnimalEndothelial CellsHumansMicedimethylaniline monooxygenase (N-oxide forming)OrnithineOxygenasesangiogenesisendothelial cell metabolismFMO2N‐acetylornithineNOTCH1

Identifiers

PMID41053533
PMCPMC12752610

What OpenQuestion holds

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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.