期刊
JOURNAL OF CELL BIOLOGY
卷 182, 期 3, 页码 459-465出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200803024
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- NIAMS NIH HHS [P01 AR048564, P01-AR048564] Funding Source: Medline
- NIDDK NIH HHS [R01 DK073944, R01 DK077276, R01 DK077276-01A1] Funding Source: Medline
- PHS HHS [R01-073944, R01-077276] Funding Source: Medline
Fibroblast growth factor 23 (FGF-23) and Klotho are secretory proteins that regulate mineral-ion metabolism. Fgf-23(-/-) or Klotho(-/-) knockout mice exhibit several pathophysiological processes consistent with premature aging including severe atrophy of tissues. We show that the signal transduction pathways initiated by FGF-23-Klotho prevent tissue atrophy by stimulating proliferation and preventing apoptosis caused by excessive systemic vitamin D. Because serum levels of active vitamin D are greatly increased upon genetic ablation of Fgf-23 or Klotho, we find that these molecules have a dual role in suppression of apoptotic actions of vitamin D through both negative regulation of 1 alpha-hydroxylase expression and phosphoinositide-3 kinase-dependent inhibition of caspase activity. These data provide new insights into the physiological roles of FGF-23 and Klotho.
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