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Endocrines, Volume 3, Issue 2

June 2022 - 14 articles

Cover Story: The excessive action of FGF23 underlies various hypophosphatemic diseases. In hereditary hypophosphatemia, such as X-linked hypophosphatemic rickets (XLH), autosomal dominant hypophosphatemic rickets (ADHR), autosomal recessive hypophosphatemic rickets 1 (ARHR1), and Raine syndrome (RNS), excessive amounts of FGF23 are produced from osteocytes with mutations. In tumor-induced osteomalacia (TIO), the responsible tumor cells overproduce FGF23. In both cases, FGF23 binds to FGF receptors (FGFRs) and aKlotho to suppress the renal expression of Na⁺/Pi cotransporters NaPi-IIa and NaPi-IIc, which increases urinary Pi excretion and causes hypophosphatemia. Moreover, FGF23 decreases the production of 1,25-dihydroxyvitamin D (1,25(OH)₂D) via the suppression of vitamin D-1a-hydroxylase (1aOHase) and the induction of vitamin D-24-hydroxylase (24OHase), which reduces the intestinal absorption of Pi. View this paper

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Endocrines - ISSN 2673-396X

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