Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process Mohammed S. Razzaque * , Despina Sitara * , Takashi Taguchi † , René St-Arnaud ‡ and Beate Lanske * ,1 * Department of Developmental Biology, Harvard School of Dental Medicine, Boston, Massachusetts, USA; † Department of Pathology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; ‡ Genetics Unit, Shriners Hospital, Montreal, Québec, Canada 1 Correspondence: Department of Developmental Biology, Harvard School of Dental Medicine, Research and Education Building, Room 303, 188 Longwood Ave., Boston, MA 02115, USA. E-mail: beate_lanske@hsdm.harvard.edu <h3>SPECIFIC AIMS</h3> We sought to determine the effects of in vivo genetic ablation of fibroblast growth factor 23 ( Fgf-23 –/– ) on premature aging and survival. Upon finding that Fgf-23 –/– mice exhibit numerous biochemical and morphological features consistent with premature aging-like phenotypes, along with severe atherosclerosis, widespread soft tissue calcifications, and increased vitamin D activities, we investigated the role of vitamin D in Fgf-23 –/– mice by ablating its activation pathway by generating Fgf-23/1α hydroxylase double mutant animals ( Fgf-23 –/– / 1α(OH)ase –/– ). Fgf-23 –/– / 1α(OH)ase –/– compound mutants, not only eliminated atherosclerosis, ectopic calcifications, and other
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Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process
Razzaque, Mohammed S.; Sitara, Despina; Taguchi, Takashi; St-Arnaud, René; Lanske, Beate
Follow The FASEB Journal
, Volume 20 (6): 720
Fed of American Socs for Experimental Biology – Apr 1, 2006
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