Urakawa, I. et al. Klotho converts canonical FGF receptor into a specific receptor for FGF23. Nature 444, 770–774 (2006).
Shimada, T. et al. FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis. J. Bone Min. Res 19, 429–435 (2004).
Farrow, E. G. et al. Iron deficiency drives an autosomal dominant hypophosphatemic rickets (ADHR) phenotype in fibroblast growth factor-23 (Fgf23) knock-in mice. Proc. Natl. Acad. Sci. USA 108, E1146–E1155 (2011).
David, V. et al. Inflammation and functional iron deficiency regulate fibroblast growth factor 23 production. Kidney Int. 89, 135–146 (2016).
Spencer, J. A. et al. Direct measurement of local oxygen concentration in the bone marrow of live animals. Nature 508, 269–273 (2014).
Harrison, J. S., Rameshwar, P., Chang, V. & Bandari, P. Oxygen saturation in the bone marrow of healthy volunteers. Blood 99, 394 (2002).
Mohyeldin, A., Garzon-Muvdi, T. & Quinones-Hinojosa, A. Oxygen in stem cell biology: a critical component of the stem cell niche. Cell Stem Cell 7, 150–161 (2010).
Rankin, E. B., Giaccia, A. J. & Schipani, E. A central role for hypoxic signaling in cartilage, bone, and hematopoiesis. Curr. Osteoporos. Rep. 9, 46–52 (2011).
Hirao, M. et al. Oxygen tension is an important mediator of the transformation of osteoblasts to osteocytes. J. Bone Miner. Metab. 25, 266–276 (2007).
Stegen, S. et al. Osteocytic oxygen sensing controls bone mass through epigenetic regulation of sclerostin. Nat. Commun. 9, 2557 (2018).
Forsythe, J. A. et al. Activation of vascular endothelial growth factor gene transcription by hypoxia-inducible factor 1. Mol. Cell. Biol. 16, 4604–4613 (1996).
Semenza, G. L. & Wang, G. L. A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. Mol. Cell. Biol. 12, 5447–5454 (1992).
Imel, E. A. et al. Iron modifies plasma FGF23 differently in autosomal dominant hypophosphatemic rickets and healthy humans. J. Clin. Endocrinol. Metab. 96, 3541–3549 (2011).
Econs, M. J. & McEnery, P. T. Autosomal dominant hypophosphatemic rickets/osteomalacia: clinical characterization of a novel renal phosphate-wasting disorder. J. Clin. Endocrinol. Metab. 82, 674–681 (1997).
White, K. E. et al. Autosomal-dominant hypophosphatemic rickets (ADHR) mutations stabilize FGF-23. Kidney Int. 60, 2079–2086 (2001).
Hum, J. M. et al. The metabolic bone disease associated with the Hyp mutation is independent of osteoblastic HIF1alpha expression. Bone Rep. 6, 38–43 (2017).
Zhang, Q. et al. The hypoxia-inducible factor-1alpha activates ectopic production of fibroblast growth factor 23 in tumor-induced osteomalacia. Bone Res. 4, 16011 (2016).
Imel, E. A., Hui, S. L. & Econs, M. J. FGF23 concentrations vary with disease status in autosomal dominant hypophosphatemic rickets. J. Bone Min. Res 22, 520–526 (2007).
Imel, E. A. et al. Oral iron replacement normalizes fibroblast growth factor 23 in iron-deficient patients with autosomal dominant hypophosphatemic rickets. J. Bone Min. Res. 35, 231–238 (2020).
Koh, N. et al. Severely reduced production of klotho in human chronic renal failure kidney. Biochem Biophys. Res Commun. 280, 1015–1020 (2001).
Hu, M. C., Kuro-o, M. & Moe, O. W. Klotho and kidney disease. J. Nephrol. 23, S136–S144 (2010).
Hu, M. C. et al. Klotho deficiency causes vascular calcification in chronic kidney disease. J. Am. Soc. Nephrol. 22, 124–136 (2011).
Hu, M. C., Shiizaki, K., Kuro-o, M. & Moe, O. W. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu. Rev. Physiol. 75, 503–533 (2013).
Babitt, J. L. & Lin, H. Y. Mechanisms of anemia in CKD. J. Am. Soc. Nephrol. 23, 1631–1634 (2012).
Noonan, M. L. et al. Erythropoietin and a hypoxia-inducible factor prolyl hydroxylase inhibitor (HIF-PHDi) lowers FGF23 in a model of chronic kidney disease (CKD). Physiol. Rep. 8, e14434 (2020).
Noonan, M. L. et al. The HIF-PHI BAY 85-3934 (Molidustat) improves anemia and is associated with reduced levels of circulating FGF23 in a CKD Mouse Model. J. Bone Min. Res. 36, 1117–1130 (2021).
Faul, C. et al. FGF23 induces left ventricular hypertrophy. J. Clin. Invest. 121, 4393–4408 (2011).
Leifheit-Nestler, M. et al. Induction of cardiac FGF23/FGFR4 expression is associated with left ventricular hypertrophy in patients with chronic kidney disease. Nephrol. Dial. Transpl. 31, 1088–1099 (2016).
Mehta, R. et al. Iron status, fibroblast growth factor 23 and cardiovascular and kidney outcomes in chronic kidney disease. Kidney Int. 100, 1292–1302 (2021).
Prideaux, M. et al. Generation of two multipotent mesenchymal progenitor cell lines capable of osteogenic, mature osteocyte, adipogenic, and chondrogenic differentiation. Sci. Rep. 11, 22593 (2021).
E. L. Clinkenbeard et al., Increased FGF23 protects against detrimental cardio-renal consequences during elevated blood phosphate in CKD. JCI Insight 4 (2019).
Onal, M. et al. A novel distal enhancer mediates inflammation-, PTH-, and early onset murine kidney disease-induced expression of the mouse Fgf23 Gene. JBMR 2, 32–47 (2018).
Ronkainen, V. P. et al. Hypoxia-inducible factor 1-induced G protein-coupled receptor 35 expression is an early marker of progressive cardiac remodelling. Cardiovasc. Res 101, 69–77 (2014).
Zhang, Y., Shi, T. & He, Y. GPR35 regulates osteogenesis via the Wnt/GSK3beta/beta-catenin signaling pathway. Biochem. Biophys. Res. Commun. 556, 171–178 (2021).
Gess, B. et al. The cellular oxygen tension regulates expression of the endoplasmic oxidoreductase ERO1-Lalpha. Eur. J. Biochem. 270, 2228–2235 (2003).
Chen, C., Li, H., Jiang, J., Zhang, Q. & Yan, F. Inhibiting PHD2 in bone marrow mesenchymal stem cells via lentiviral vector-mediated RNA interference facilitates the repair of periodontal tissue defects in SD rats. Oncotarget 8, 72676–72699 (2017).
Imel, E. A. et al. Serum fibroblast growth factor 23, serum iron and bone mineral density in premenopausal women. Bone 86, 98–105 (2016).
Wolf, M., Koch, T. A. & Bregman, D. B. Effects of iron deficiency anemia and its treatment on fibroblast growth factor 23 and phosphate homeostasis in women. J. Bone Min. Res. 28, 1793–1803 (2013).
Haase, V. H. HIF-prolyl hydroxylases as therapeutic targets in erythropoiesis and iron metabolism. Hemodial. Int. 21, S110–S124 (2017).
Yeh, T. L. et al. Molecular and cellular mechanisms of HIF prolyl hydroxylase inhibitors in clinical trials. Chem. Sci. 8, 7651–7668 (2017).
Clinkenbeard, E. L. et al. Erythropoietin stimulates murine and human fibroblast growth factor-23, revealing novel roles for bone and bone marrow. Haematologica 102, e427–e430 (2017).
Hanudel, M. R. et al. Effects of erythropoietin on fibroblast growth factor 23 in mice and humans. Nephrol. Dial. Transpl. 34, 2057–2065 (2018).
Daryadel, A. et al. Erythropoietin stimulates fibroblast growth factor 23 (FGF23) in mice and men. Pflug. Arch. 470, 1569–1582 (2018).
Kwon, S. Y. et al. Hypoxia enhances cell properties of human mesenchymal stem cells. Tissue Eng. Regen. Med 14, 595–604 (2017).
Antebi, B. et al. Short-term physiological hypoxia potentiates the therapeutic function of mesenchymal stem cells. Stem Cell. Res. Ther. 9, 265 (2018).
Wang, Y. et al. The hypoxia-inducible factor alpha pathway couples angiogenesis to osteogenesis during skeletal development. J. Clin. Invest. 117, 1616–1626 (2007).
Hung, S. P., Ho, J. H., Shih, Y. R., Lo, T. & Lee, O. K. Hypoxia promotes proliferation and osteogenic differentiation potentials of human mesenchymal stem cells. J. Orthop. Res. 30, 260–266 (2012).
Wu, C. et al. Oxygen-sensing PHDs regulate bone homeostasis through the modulation of osteoprotegerin. Genes Dev. 29, 817–831 (2015).
留言 (0)