FGF23depend

FGF23depend is a term used in physiology and nephrology to denote biological states or models in which cellular or systemic processes rely predominantly on signaling by fibroblast growth factor 23 (FGF23). In this framing, a tissue, cell type, or experimental condition is described as FGF23dependent when its activity or phenotype changes primarily in response to FGF23 signaling, as opposed to signals from other regulators of phosphate and vitamin D metabolism.

FGF23 acts mainly on the kidney, requiring the Klotho co-receptor and FGF receptors to suppress the sodium-phosphate co-transporters NaPi-IIa and NaPi-IIc, reduce 1α-hydroxylase activity, and increase 24-h-hydroxylase activity, leading to lower phosphate reabsorption and decreased active vitamin D. In FGF23dependent contexts, the magnitude of these effects tracks with circulating FGF23 levels and tissue sensitivity, which can be influenced by Klotho expression, receptor availability, and downstream signaling components. The concept emphasizes how reliance on FGF23 signaling shapes metabolic outcomes.

Clinically, FGF23depend is discussed in relation to disorders of phosphate handling and mineral metabolism, such as chronic kidney disease and certain genetic phosphate-wasting conditions. Researchers may categorize models or patient samples by their reliance on FGF23 signaling to explain phosphate balance, vitamin D status, or bone mineralization, and to evaluate responses to FGF23-targeted therapies or alternative regulatory pathways.

Assessment of FGF23depend relies on measuring circulating FGF23, receptor and co-receptor expression, and functional readouts like phosphate excretion and vitamin D metabolites, often alongside genetic or pharmacologic manipulation. Limitations include redundancy with other phosphaturic factors and FGF23-independent pathways regulating mineral metabolism. See also FGF23, Klotho, phosphate homeostasis.