ArticleInternational dental journal2024
Diabetic Macrophage Exosomal miR-381-3p Inhibits Epithelial Cell Autophagy Via NR5A2.
Article in International dental journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Identification of exosomal miRNA-based predictive signatures for gestational diabetes mellitus via multi-algorithm machine learning.BMC pregnancy and childbirth · 2026Article
- Exosomal microRNAs in Periodontitis: From Molecular Footprints to Clinical Frontiers.ACS pharmacology & translational science · 2026Review
- Engineering MSC-exosomes for diabetic bone regeneration: from mechanism to delivery.Stem cell research & therapy · 2026Review
- Autophagy-Ferroptosis Interplay Network: Redefining Therapeutic Paradigms for Diabetic Wound Healing.Journal of inflammation research · 2026Review
- Exosomes as Central Mediators of Host-Pathogen Interactions in Periodontitis: A Systematic Literature Review.Cureus · 2025Review
- The Role of Autophagy in the Regulation of Bidirectional Relationships in Diabetic Periodontitis.Journal of inflammation research · 2025Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo explore the mechanism underlying autophagy disruption in gingival epithelial cells (GECs) in diabetic individuals. METHODS AND MATERIALS: Bone marrow-derived macrophages (BMDMs) and GECs were extracted from C57/bl and db/db mice, the exosomes (Exo) were isolated from BMDMs. qRT‒PCR and Western blotting were performed to analyse gene expression. The AnimalTFDB database was used to identify relevant transcription factors, and miRNA sequencing was utilised to identify relevant miRNAs with the aid of the TargetScan/miRDB/miRWalk databases. A dual-luciferase assay was conducted to verify intermolecular targeting relationships.
resultsSimilar to BMDMs, BMDM-derived Exos disrupted autophagy and exerted proinflammatory effects in GEC cocultures, and ATG7 may play a vital role. AnimalTFDB database analysis and dual-luciferase assays indicated that NR5A2 is the most relevant transcription factor that regulates Atg7 expression. SiRNA-NR5A2 transfection blocked autophagy in GECs and exacerbated inflammation, whereas NR5A2 upregulation restored ATG7 expression and ameliorated Exo
conclusionBMDM-derived Exos, which carry miR-381-3p, inhibit NR5A2 and disrupt autophagy in GECs, increasing periodontal inflammation in diabetes.
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