ArticleAngiogenesis2026
YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.
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.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
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
Identifiers
42776305What Socratic holds
Registered trials
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.