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Role of Klotho in bone and implication for CKD.
Hirotaka Komaba1,2,3, Beate Lanske4
1Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine.
Current Opinion in Nephrology and Hypertension
|April 27, 2018
Summary
Bone Klotho protein regulates bone metabolism and fibroblast growth factor 23 (FGF23) production. Loss of bone Klotho increases bone volume, but this may be offset by kidney failure, impacting therapies for renal osteodystrophy.
Area of Science:
- Endocrinology
- Bone Biology
- Mineral Metabolism
Background:
- Klotho is a transmembrane protein functioning as a co-receptor for FGF23.
- Klotho has been identified in bone cells, including osteoblasts and osteocytes.
- This suggests bone as a potential target organ for FGF23.
Purpose of the Study:
- To review the emerging literature on the roles of bone Klotho in mineral and bone metabolism.
- To discuss the involvement of bone Klotho in renal osteodystrophy.
Main Methods:
- Review of recent scientific literature.
- Analysis of mouse genetic studies on Klotho function in bone.
- Discussion of FGF23 and Wnt signaling pathways in bone.
Main Results:
- Loss of Klotho in osteocytes leads to increased bone formation and volume in mice.
- FGF23 exhibits autocrine/paracrine functions in regulating its own production and Wnt-mediated bone formation.
- Down-regulation of bone Klotho in renal failure may counteract these effects.
Conclusions:
- Bone Klotho plays a crucial role in bone formation and FGF23 regulation.
- Further research is needed to develop therapeutic strategies for bone fragility in renal osteodystrophy.
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