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See Latest ArticlesIs there a role for NFAT inhibitors in the prevention of bone destruction
HSS Journal (Musculoskeletal Journal of Hospital for Special Surgery), 05/19/09
McMahon MS – Pathologic conditions resulting from excessive bone destruction include osteoporosis, rheumatoid arthritis, metastases, periprosthetic osteolysis, cherubism, and others. This review article summarizes the metabolic pathways known to be involved in this pathology. The immunosuppressive drugs, Cyclosporin A and Tacrolimus, inhibit osteoclast formation by targeting the NFAT/calcineurin pathway.
- RANKL-RANK–calcineurin–NFAT–calcineurin/NFAT complex enters nucleus—activates osteoclast DNA
- In treated cells, the pathway becomes: RANKL–RANK–calcineurin–Cyclosporin A inhibits calcineurin–NFAT–calcineurin/NFAT complexes do not form—NFAT remains in cytoplasm—osteoclast DNA not activated
- These NFAT inhibitors should be considered in the treatment of osteoclastic hyper-resorptive syndromes
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