Related Experiment Video
Updated: May 3, 2026
5/6th Nephrectomy in Combination with High Salt Diet and Nitric Oxide Synthase Inhibition to Induce Chronic Kidney Disease in the Lewis Rat
Published on: July 3, 2013
Can targeting the FGF23-αKlotho signaling system delay phosphate-driven organ damage?
Mohammed S Razzaque1, Moosa Mohammadi2
1Department of Medical Education, School of Medicine, University of Texas Rio Grande Valley (UTRGV), Edinburg, TX, USA.
Introduction:
Inexorable high serum phosphate levels in chronic kidney disease (CKD) patients deteriorate the functionality of the musculoskeletal, renal, and cardiovascular systems, thereby contributing to increased morbidity and mortality. Higher phosphate balance has also been correlated with increased mortality rates in individuals with normal renal function, independent of other comorbidities. Clinical and epidemiological studies of CKD patients and healthy subjects, alongside evidence of accelerated aging in murine models induced by excessive phosphate loading, indicate that phosphate toxicity is a driver of premature aging and age-related organ damage.
Area Covered:
This article briefly discusses the causes and consequences of phosphate toxicity in the context of organ damage and aging while also elaborating on the therapeutic potential of the fibroblast growth factor 23 (FGF23) hormone signaling system in alleviating phosphate toxicity in patients with normal kidney function and CKD.
Expert Opinion:
Human age-associated disorders may be delayed through dietary programs or pharmacological interventions capable of modulating the activity of FGF23 signaling to reduce the systemic phosphate burden.
