IL-1β Drives Production of FGF-23 at the Onset of Chronic Kidney Disease in Mice.

Journal of Bone and Mineral Research : the Official Journal of the American Society for Bone and Mineral Research
Quiana McKnightJackie A Fretz

Abstract

FGF-23 has arisen as an early biomarker of renal dysfunction, but at the onset of chronic kidney disease (CKD), data suggest that FGF-23 may be produced independently of the parathyroid hormone (PTH), 1,25(OH)2 -vitamin D3 signaling axis. Iron status is inversely correlated to the level of circulating FGF-23, and improvement in iron bioavailability within patients correlates with a decrease in FGF-23. Alternately, recent evidence also supports a regulatory role of inflammatory cytokines in the modulation of FGF-23 expression. To determine the identity of the signal from the kidney-inducing upregulation of osteocytic FGF-23 at the onset of CKD, we utilized a mouse model of congenital CKD that fails to properly mature the glomerular capillary tuft. We profiled the sequential presentation of indicators of renal dysfunction, phosphate imbalance, and iron bioavailability and transport to identify the events that initiate osteocytic production of FGF-23 during the onset of CKD. We report here that elevations in circulating intact-FGF-23 coincide with the earliest indicators of renal dysfunction (P14), and precede changes in serum phosphate or iron homeostasis. Serum PTH was also not changed within the first month. Instead, production...Continue Reading

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Citations

Nov 26, 2020·International Journal of Molecular Sciences·Maria L MaceEwa Lewin
Jan 3, 2021·Pediatric Nephrology : Journal of the International Pediatric Nephrology Association·Kelly MezaOleh Akchurin
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Nov 11, 2021·Current Osteoporosis Reports·Petra Simic, Jodie L Babitt

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