Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process.

Authors: Razzaque MS; Sitara D; Taguchi T; St-Arnaud R; Lanske B
Year: 2006
Journal: FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Abstract: Fibroblast growth factor 23 null mice (Fgf-23-/-) have a short lifespan and show numerous biochemical and morphological features consistent with premature aging-like phenotypes, including kyphosis, severe muscle wasting, hypogonadism, osteopenia, emphysema, uncoordinated movement, T cell dysregulation, and atrophy of the intestinal villi, skin, thymus, and spleen. Furthermore, increased vitamin D activities in homozygous mutants are associated with severe atherosclerosis and widespread soft tissue calcifications; ablation of vitamin D activity from Fgf-23-/- mice, by genetically deleting the 1alpha(OH)ase gene, eliminates atherosclerosis and ectopic calcifications and significantly rescues premature aging-like features of Fgf-23-/- mice, resulting in prolonged survival of Fgf-23-/-/1alpha(OH)ase-/- double mutants. Our results indicate a novel role of Fgf-23 in developing premature aging-like features through regulating vitamin D homeostasis. Finally, our data support a new model of interactions among Fgf-23, vitamin D, and klotho, a gene described as being associated with premature aging process.
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Created on Jan. 3, 2013, 6:26 p.m.
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Integrated: False

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Species: House mouse

Experiments: 0
Interventions:

Fgf23 knockout

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