Journal: Frontiers in Pharmacology
Article Title: DNA methylation and immune regulation in osteoporosis: emerging epigenetic targets for drug discovery
doi: 10.3389/fphar.2025.1688305
Figure Lengend Snippet: The Triad of Osteoporosis: Pathophysiology, Molecular Pathways, and Treatment Approaches. From healthy bones to the development of osteoporosis. It integrates various factors: aging, hormonal abnormalities, inflammation, etc. It involves multi-layered mechanisms: from immune-bone interaction regulation to epigenetic regulation mediated by DNA methylation, analyzing the molecular mechanisms of bone metabolism disorders. Specifically, DNA methylation mediated by DNMT1/3A/3B exerts dual regulatory effects: on one hand, it targets and modulates key bone metabolism-related genes such as Runx2, SOST, and NFATc1, as well as signaling pathways including RANKL/RANK and Wnt/β-Catenin; on the other hand, it influences immune-osseous signaling pathways involving M1/M2 macrophages, T cells, IL-1RN, and NF-κB. Both regulatory effects ultimately drive the imbalance between bone resorption and bone formation. It covers multiple therapeutic strategies: various existing treatments, the potential use of DNMTi. And correlates bone turnover markers (BTM) with the diagnostic value of DNA methylation biomarkers.
Article Snippet: (Cell Death Dis) , Mouse and human cells , NFATc1 (RNA m6A; METTL14/YTHDF2) , Exosome-delivered METTL14 ↑ m6A at NFATc1 (4249A) → mRNA decay , Inhibits osteoclast resorption, preserves bone , .
Techniques: DNA Methylation Assay, Protein-Protein interactions, Diagnostic Assay