Fibroblast Growth Factor 23-Mediated Bone Disease.
Anda R Gonciulea1, Suzanne M Jan De Beur1
1Division of Endocrinology, Diabetes and Metabolism, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Fibroblast growth factor 23 (FGF23) regulates phosphate and vitamin D metabolism. Dysregulation of FGF23 causes skeletal disorders, reviewed here with its signaling pathway and associated conditions.
Area of Science:
- Endocrinology
- Metabolic Bone Disease
- Molecular Biology
Background:
- Fibroblast growth factor 23 (FGF23) is a key hormone controlling phosphate and vitamin D homeostasis.
- Imbalances in FGF23 levels are linked to numerous skeletal pathologies.
- The FGF23-α-Klotho axis is crucial for these metabolic functions.
Purpose of the Study:
- To review the FGF23-α-Klotho signaling pathway.
- To highlight recent advancements in FGF23 regulation and function.
- To describe skeletal disorders stemming from FGF23 dysregulation.
Main Methods:
- Literature review of FGF23 research.
- Analysis of FGF23-α-Klotho pathway mechanisms.
- Synthesis of clinical data on FGF23-related disorders.
Main Results:
- Detailed overview of FGF23 synthesis, secretion, and target organ actions.
- Explanation of the role of α-Klotho as a co-receptor for FGF23.
- Summarization of genetic and acquired conditions associated with FGF23 excess or deficiency.
Conclusions:
- The FGF23-α-Klotho pathway is central to mineral metabolism.
- Understanding FGF23 regulation and signaling is vital for diagnosing and managing skeletal disorders.
- Further research into FGF23 may reveal novel therapeutic targets.
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