Abstract
Osteoporosis is a chronic debilitating disease caused by imbalanced bone remodeling processes that impair the structural integrity of bone. Over the last ten years, the association between fibroblast growth factor 23 (FGF23) and osteoporosis has been studied in both pre-clinical and clinical investigations. FGF23 is a bone-derived endocrine factor that regulates mineral homeostasis via the fibroblast growth factor receptors (FGFRs)/αKlotho complex. These receptors are expressed in kidney and the parathyroid gland. Preclinical studies have supported the link between the local actions of FGF23 on the bone remodeling processes. In addition, clinical evidence regarding the effects of FGF23 on bone mass and fragility fractures suggest potential diagnostic and prognostic applications of FGF23 in clinical contexts, particularly in elderly and patients with chronic kidney disease. However, inconsistent findings exist and there are areas of uncertainty requiring exploration. This review comprehensively summarizes and discusses preclinical and clinical reports on the roles of FGF23 on osteoporosis, with an emphasis on the local action, as opposed to the systemic action, of FGF23 on the bone. Current gaps in knowledge and future research directions are also suggested to encourage further rigorous research in this important field.
Highlights
Osteoporosis is a chronic debilitating disease caused by an imbalance in bone remodeling processes that favor bone resorption over bone formation
The fibroblast growth factor 23 (FGF23)-mediated mechanism interacts with the classical calcium/phosphate regulating processes driven by parathyroid hormone (PTH) and calcitriol
Despite the fact that FGF23 significantly inhibits PTH production and secretion, the dominant regulators of PTH levels remain at circulating free calcium and calcitriol levels, which are monitored by the calcium-sensing receptor (CaSR) and the VDR in the parathyroid gland [17,18]
Summary
Osteoporosis is a chronic debilitating disease caused by an imbalance in bone remodeling processes that favor bone resorption over bone formation. FGF23 is a bone-derived endocrine factor that regulates phosphate and vitamin D homeostasis via the fibroblast growth factor receptors (FGFRs)/αKlotho complex These receptors are expressed in kidney and the parathyroid gland [5,6,7]. Accumulating evidence from clinical studies reported the association between FGF23, bone remodeling and fragility fracture in the elderly, either with or without a decline in renal function. These recent advances in the insights regarding FGF23 effects in mineral homeostasis and bone remodeling suggest potential clinical applications of FGF23 in the clinical context. Current gaps in knowledge and future research directions are suggested to encourage further rigorous research in this important field
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