Unravelling the Molecular Footprints of Diabetic Foot Ulcers: In Silico Discovery of Key Protein and MicroRNA Signatures

Diabetic foot ulcers (DFUs) present a significant clinical challenge, characterized by chronic inflammation and impaired wound healing. This study employs Gene Ontology (GO) analysis to identify critical biological processes, molecular functions, cellular components, and pathways associated with DFUs, aiming to uncover novel therapeutic targets. The analysis reveals significant enrichment in biological processes such as Positive Regulation of miRNA Transcription and Regulation of miRNA Transcription, highlighting the crucial role of microRNAs, including hsa-miR-34a-5p, hsa-miR-155-5p, hsa-miR-17-5p, hsa-miR-29b-3p, hsa-miR-7-5p, hsa-miR-1-3p, and hsa-miR-23b-3p, in regulating wound healing and inflammation. Enriched molecular functions, such as DNA-binding Transcription Activator Activity and Protein Phosphatase Binding, suggest that targeting genes like TP53, GAPDH, AKT1, MYC, TNF, EGFR, STAT3, FN1, VEGFA, and JUN could modulate critical cellular processes and improve DFU management. The analysis also identifies key cellular components, including Vesicle and Platelet Alpha Granule Lumen, as crucial for cellular transport and signaling, suggesting that interventions targeting these components could enhance wound repair. Furthermore, enriched pathways such as Proteoglycans in Cancer and Human Cytomegalovirus Infection indicate potential mechanisms and viral influences relevant to DFUs. These findings provide a comprehensive framework for developing targeted therapies that address the multifaceted pathology of DFUs, offering promising avenues for improving patient outcomes and advancing wound healing strategies.