METTL16 Identified as Key Regulator in Diabetic Foot Ulcer via m6A Methylation
Summary: Using integrated bioinformatics and multiple machine learning algorithms (LASSO, SVM-RFE, GBM), researchers identified 12 differentially expressed m6A-related genes in DFU tissues. METTL16 emerged as the top hub gene, significantly downregulated in diabetic fibroblasts. Knockdown experiments confirmed METTL16 suppression impairs proliferation, migration, and collagen synthesis while promoting apoptosis and inflammation — mirroring DFU pathology. Overexpression partially rescued these defects. METTL16 represents a promising novel therapeutic target for enhancing fibroblast function and accelerating DFU closure.
Key Highlights:
- Methods: RNA-seq + WGCNA + LASSO/SVM-RFE/GBM algorithms.
- Hub Gene: METTL16 (downregulated in DFU).
- Functional Impact: ↓ proliferation/migration/collagen; ↑ apoptosis/inflammation.
- Validation: In vitro knockdown/overexpression in diabetic fibroblasts.
- Authors: Multiple (bioinformatics + experimental team).
Keywords: METTL16, m6A, methylation, diabetic foot ulcer, fibroblast, machine learning