Evidence map›Paper›PMID 42776305›Full record

ArticleAngiogenesis2026

YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.

Xiaosa Li, Jiale Wang, Liang Yuan, Yuqi Wang, Jinzhi Wei, Ping Li, Runxin Wang, Xingyan Xu, Qiuwen Mai, Junxiu Liu and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Angiogenesis, 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

12 authors.

Xiaosa Li *Department of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Jiale Wang *Department of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Liang Yuan *Sino-French Hoffmann Institute, School of Basic Medical Science, Guangzhou Medical University, Guangzhou, 510260, China.
Yuqi WangDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Jinzhi WeiDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Ping LiDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Runxin WangDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Xingyan XuDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China.
Qiuwen MaiDepartment of Obstetricsand Gynecology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Junxiu LiuDepartment of Obstetricsand Gynecology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. liujxiu@mail.sysu.edu.cn.
Huiping LinDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China. 2021390022@gzhmu.edu.cn.
Xiaodong FuDepartment of Cardiology, Guangdong Key Laboratory of Vascular Diseases, The Second Affiliated Hospital, Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, 510260, China. fuxiaod@gzhmu.edu.cn.

Funding

the National Natural Science Foundation of China 82171631the National Special Fund for Basic and Applied Basic Research of Guangzhou 2024A04J4653
6 · The paper itself

Abstract

Angiogenesis plays a critical role in the progression of endometriosis, with enhanced glycolysis accelerating pathological angiogenesis. Prior research has identified a central role for N6-methyladenosine (m6A) modification in regulating glycolytic processes. This study investigates the involvement of m6A-mediated mechanisms in the regulation of glycolysis and angiogenesis in endometriosis. Here, we report that PFKFB3 is significantly upregulated in vascular endothelial cells of ectopic endometrial tissues from humans and mice, correlating with elevated expression of YTHDF3. Specific deletion of Ythdf3 in endothelial cells reduces PFKFB3 protein levels and suppresses angiogenesis in ectopic endometrial lesions. Mechanistically, PFKFB3 mRNA displays increased m6A modifications in endometrial microvascular endothelial cells (EMECs). METTL3 enhances m6A modification of PFKFB3 mRNA, which is recognized by YTHDF3, promoting PFKFB3 translation and glycolytic activity, thus facilitating tube formation, migration, and proliferation of ovarian microvascular endothelial cells (OMECs). Moreover, estrogen upregulates both METTL3 and PFKFB3 via the estrogen receptor ERα. Collectively, these findings establish the YTHDF3-m6A-PFKFB3 pathway as a critical driver of angiogenesis in endometriosis, suggesting that targeting this pathway represents a promising therapeutic strategy.

Indexed as

EndometriosisNeovascularization, PathologicPhosphofructokinase-2Protein BiosynthesisRNA-Binding ProteinsAdenosineAnimalsCell MovementCell ProliferationEndometriumEndothelial CellsFemaleGlycolysisHumansMethyltransferasesMiceAdenosineMethyltransferasesN-methyladenosinePFKFB3 protein, humanPFKFB3 protein, mousePhosphofructokinase-2RNA-Binding ProteinsYTHDF3 protein, humanAngiogenesisEndometriosisGlycolysisN6-methyladenosinePFKFB3YTHDF3

Identifiers

What Socratic holds

Textmetadata
Read underepoch 390

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 Socratic graph.