ArticleEuropean journal of medical research2025
METTL14-mediated m6A methylation promotes macrophage M2 polarization via YTHDF1-Socs1 axis to accelerate skin wound healing.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.International journal of biological sciences · 2026Review
- RNA modifications: molecular orchestrators of wound healing.Burns & trauma · 2026Article
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Authors and funding
3 authors.
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Abstract
backgroundMacrophage polarization plays a crucial role in the processes of inflammation, angiogenesis, and wound healing. N6-methyladenosine (m
methodsA full-thickness skin wounds mouse model was established and treated with Socs1 overexpression. The wound healing process and the histological changes of skin tissues were detected. Ana-1 macrophages were treated with lipopolysaccharide (LPS) to mimic the inflammatory environment during the wound healing process. The macrophage polarization was detected by immunofluorescence staining of specific biomarkers and production of inflammatory factors was measured using ELISA kits. Angiogenesis and fibroblast proliferation and migration were measured by the co-culture system of Ana-1 with dermal microvascular endothelial cells (DMECs) or dermal fibroblasts (DFs). The m
resultsSocs1 expression was upregulated during wound healing process and M2 polarization of macrophages. Socs1 overexpression accelerated mouse skin wound healing and enhanced the formation of granulation tissue in wound tissues. Co-culture with Socs1-overexpressed macrophages increased angiogenesis of DMECs and enhanced the viability and migration of DFs. METTL14 regulates Socs1 expression in Ana-1 cells and increased the m
conclusionSocs1 regulates the M2 macrophages polarization and accelerates wound healing, which is modulated by METTL14-mediated m
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