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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Curr+Opin+Nephrol+Hypertens
2016 ; 25
(4
): 333-42
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Multiple faces of fibroblast growth factor-23
#MMPMID27219044
Han X
; Quarles LD
Curr Opin Nephrol Hypertens
2016[Jul]; 25
(4
): 333-42
PMID27219044
show ga
PURPOSE OF REVIEW: This review examines the role of fibroblast growth factor-23
(FGF-23) in mineral metabolism, innate immunity and adverse cardiovascular
outcomes. RECENT FINDINGS: FGF-23, produced by osteocytes in bone, activates
FGFR/?-Klotho (?-Kl) complexes in the kidney. The resulting bone-kidney axis
coordinates renal phosphate reabsorption with bone mineralization, and creates a
counter-regulatory feedback loop to prevent vitamin D toxicity. FGF-23 acts to
counter-regulate the effects of vitamin D on innate immunity and cardiovascular
responses. FGF-23 is ectopically expressed along with ?-Kl in activated
macrophages, creating a proinflammatory paracrine signaling pathway that counters
the antiinflammatory actions of vitamin D. FGF-23 also inhibits
angiotensin-converting enzyme 2 expression and increases sodium reabsorption in
the kidney, leading to hypertension and left ventricular hypertrophy. Finally,
FGF-23 is purported to cause adverse cardiac and impair neutrophil responses
through activation of FGFRs in the absence of ?-Kl. Although secreted forms of
?-Kl have FGF-23 independent effects, the possibility of ?-Kl independent effects
of FGF-23 is controversial and requires additional experimental validation.
SUMMARY: FGF-23 participates in a bone-kidney axis regulating mineral
homeostasis, proinflammatory paracrine macrophage signaling pathways, and in a
bone-cardio-renal axis regulating hemodynamics that counteract the effects of
vitamin D.
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