ArticleFrontiers in pharmacology2025
Exosomal miR-93-3p targets EIF4EBP1 to regulate macrophage polarization and accelerate wound healing post-anal fistula surgery.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Exosomes orchestrate immune homeostasis in acute ischemia-reperfusion flap injury and chronic wounds: the TLR4/NF-κB-STAT3 R-ratio balance decision model, engineering optimization and translational clinical strategy.Frontiers in immunology · 2026Pooled it
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Pathological neutrophil extracellular traps hinder postoperative anal fistula wound healing and are attenuated by Zuoqing granule via suppression of the Nox4 pathway.Frontiers in immunology · 2025Article
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5 authors.
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Abstract
Background: Delayed wound healing following anal fistula (AF) surgery remains a clinical challenge. This study endeavors to identify and validate key exosomal miRNAs that regulate postoperative inflammation after AF surgery by integrating multi-omics analyses with functional assays, and to elucidate the molecular mechanisms by which these miRNAs and their target genes influence macrophage M1/M2 polarization. Methods: 15 patients undergoing AF surgery were randomized to three groups. The negative control group received sterile Vaseline gauze dressings, the positive control cohort took Kangfuxin Solution, and the treatment cohort received Wugu Qilin Ointment. Wound exudates were collected postoperatively and exosomes were isolated via ultracentrifugation. Total RNA was extracted through the TRIzol method, followed by miRNA microarray analysis to identify differentially expressed miRNAs (DEMs). Candidate miRNAs were validated via qPCR to identify those significantly linked to the therapeutic efficacy of the traditional Chinese medicine (TCM) method of Euriching Pus for Tissue Growth. Results: Microarray analysis and qPCR validation identified miR-93-3p as the most significantly DEMs. miR-93-3p overexpression markedly downregulated M1 macrophage marker CD86 and pro-inflammation cytokines IL-1β, IL-6, and TNF-α, while upregulating M2 markers Arg-1, CD206, and anti-inflammation cytokines IL-10 and TGF-β in functional assays. Conversely, miR-93-3p suppression exhibited the opposite effect. WB analysis confirmed that miR-93-3p bidirectionally regulated CD86, Arg-1, and CD206 protein expression. Bioinformatic analysis suggested that miR-93-3p possibly targets EIF4EBP1, thereby modulating biological processes like inflammatory response, cellular metabolism, and MP. This regulatory relationship was unveiled through DLR assays, proving that miR-93-3p specifically suppresses EIF4EBP1 expression. Conclusion: This study is the first to elucidate the molecular mechanism by which the TCM therapeutic approach of Euriching Pus for Tissue Growth promotes M2 MP through the exosomal miR-93-3p/EIF4EBP1 axis, and theoretically supports the formulation of new exosome-based miRNA treatment strategies for postoperative anti-inflammatory treatment in AF.
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