Network pharmacology and bioinformatics analyses indicate a potential anti-aging effect of deferoxamine in mesenchymal stem cells

Aging increases health risks, particularly cardiovascular diseases, neurological disorders, and cancer. Elderly individuals experience complications from polypharmacy, underscoring the need for innovative therapies. Mesenchymal stem cells (MSCs) are promising in regenerative medicine but decline in number and function with age. This decline is exacerbated by non-heme iron accumulation, leading to cellular damage. Reducing iron may enhance MSCs function in the elderly, with deferoxamine mesylate (DFO), an iron chelator, potentially alleviating oxidative damage. This study employed network pharmacology and bioinformatics to explore DFO’s effects on aged MSCs. Target genes of DFO were obtained from the PharmMapper server, while aging-related MSCs genes were sourced from four databases. Functional enrichment, protein-protein interaction network construction, and hub gene identification were performed, with validation using the GSE35959 and GSE68374 microarray datasets from the Gene Expression Omnibus (GEO) database. A total of 148 common genes associated with the aging of MSCs treated with DFO were identified. Validation revealed that DFO significantly impacts key pathways, including the Rap1 and PI3K-Akt signaling pathways. Additionally, 13 primary target genes involved in the regulation of cell cycle and division were identified. Notably, 7 of these genes exhibited similar expression patterns in both in vitro and in vivo studies, suggesting they could be crucial for MSCs aging and primary targets of DFO. These findings shed light on DFO’s mechanisms for enhancing MSCs function and delaying aging, providing a foundation for future therapeutic strategies aimed at promoting repair and regeneration in aging populations.