Targeting CYP24A1

Allison, Susan J.

doi:10.1038/nrneph.2016.16

Research Highlight
Published: 08 February 2016

Mineral and bone disorders

Targeting CYP24A1

Susan J. Allison

Nature Reviews Nephrology volume 12, page 196 (2016)Cite this article

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Disturbed phosphate homeostasis is a common feature of chronic kidney disease (CKD). High serum levels of FGF-23 are associated with adverse effects on bone metabolism. New findings suggest that inhibition of the vitamin D-inactivating enzyme, CYP24A1, might present a new therapeutic opportunity for the treatment of mineral abnormalities associated with high FGF-23 levels.

FGF-23 regulates mineral metabolism through a series of complex pathways. Its effects on vitamin D are twofold: it inhibits the production of active 1,25[OH]₂D by downregulating CYP27B1, the enzyme responsible for 1,25[OH]₂D production, while promoting the catabolism of active 1,25[OH]₂D by upregulating CYP24A1.

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References

Bai, X. et al. CYP24 inhibition as a therapeutic target in FGF23-mediated renal phosphate wasting disorders. J. Clin. Invest. http://dx.doi.org/10.1172/JCI81928

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