Commentary 10.1172/JCI122046

The good and the bad of vitamin D inactivation

Marie B. Demay

Endocrine Unit, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Address correspondence to: Marie B. Demay, Endocrine Unit, Thier 11, Massachusetts General Hospital, 50 Blossom St., Boston, Massachusetts 02114, USA. Phone: 617.726.3966; Email: demay@helix.mgh.harvard.edu.

Find articles by Demay, M. in: JCI | PubMed | Google Scholar | Orcid 24x24

First published August 6, 2018 - More info

Published in Volume 128, Issue 9 on August 31, 2018
J Clin Invest. 2018;128(9):3736–3738. https://doi.org/10.1172/JCI122046.
Copyright © 2018, American Society for Clinical Investigation

First published August 6, 2018 - Version history

While disorders of impaired vitamin D activation and action have long been appreciated, the consequences of abnormalities in pathways leading to the inactivation of vitamin D metabolites have only recently been identified. Two recent articles have shed new light on this area of vitamin D biology. The report by Martineau et al., published in the JCI, describes a pathway in which binding of the vitamin D metabolite 24R,25(OH)2D3 to its effector molecule FAM57B2 plays an important role in endochondral ossification during bone repair. This work follows, and adds to, another recent JCI publication by Roizen et al., showing that rapid inactivation of vitamin D metabolites causes vitamin D deficiency, leading to vitamin D–dependent rickets.

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