ArticleApplied biochemistry and biotechnology2025
METTL14/YTHDF2 m6A Axis Protects Against M2 Macrophage Polarization in Endometriosis by Regulating KLF4 Stability.
Article in Applied biochemistry and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- METTL14-mediated m6A methylation promotes macrophage M2 polarization via YTHDF1-Socs1 axis to accelerate skin wound healing.European journal of medical research · 2025Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (EMs) is a chronic inflammatory disorder featured by infertility and pain. The role of N6-methyladenosine (m6A) in EMs has been evidenced. This study investigated the molecular mechanism of METTL14-m6A-KLF4 modulating macrophage polarization in EMs. RT-qPCR assay was conducted to test METTL14 levels in tissues and cells and the relative mRNA levels of M2 (Arg-1, Fizz1) and M1 (iNOS, IL-1β) factors in the supernatant after co-culture of macrophages with normal endometrial stromal cells (nESCs) or ectopic endometrial stromal cells (eESCs). CD206 and CD86 expression, as well as Arg-1, IL-10, and IL-4 levels, were assessed. Meanwhile, the relationship between METTL14 and the m6A modification of KLF4 was analyzed. Additionally, the effect of KLF4-activated M2 macrophages on in vitro ESC progression was observed. Cellular and tissue METTL14 was under-expressed in EMs. METTL14 expression might be related to macrophage M2 polarization. Co-culture of eESCs overexpressing METTL14 and macrophages downregulated Arg-1, Fizz1, CD206, IL-10, and IL-4 levels. Mechanistically, METTL14 could mediate KLF4 m6A modification through the m6A reading protein YTHDF2. KLF4 overexpression could nullify METTL14 re-expression-repressed M2 macrophage polarization. In addition, KLF4-activated M2 macrophages accelerated the proliferation and migration of ESCs in vitro. METTL14-m6A-KLF4 regulated macrophage polarization in EMs.
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Registered trials
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