Extrarenal effects of FGF23.

Area of Science:

• Nephrology
• Cardiology
• Neurology
• Immunology

Background:

• Chronic kidney disease (CKD) elevates fibroblast growth factor 23 (FGF23) and reduces its co-receptor Klotho.
• Elevated FGF23 is linked to increased mortality and cardiovascular disease risk in CKD patients.
• The physiological role of FGF23 in phosphate homeostasis is well-established, but its extrarenal effects are increasingly recognized.

Purpose of the Study:

• To review recent clinical and experimental data on the extrarenal effects of FGF23.
• To elucidate the impact of FGF23 on the cardiovascular, central nervous, and immune systems in CKD.
• To highlight FGF23 as a potential therapeutic target for CKD complications.

Main Methods:

• Literature review of clinical and experimental studies.
• Analysis of data on FGF23's molecular pathways and physiological impacts.
• Synthesis of findings related to FGF23's effects on cardiovascular, neurological, and immune functions.

Main Results:

• FGF23 directly induces left ventricular hypertrophy via the FGF receptor 4 pathway.
• FGF23 impacts hippocampal neurons, potentially impairing learning and memory in CKD.
• FGF23 directly affects immune cells, including polymorphonuclear leukocytes and macrophages.

Conclusions:

• FGF23 exerts significant extrarenal effects impacting multiple organ systems in CKD.
• Understanding these effects is crucial for managing cardiovascular, cognitive, and immune complications of CKD.
• Targeting FGF23 may offer novel therapeutic strategies for CKD patients.