Fibroblast Growth Factor 23 and Muscle Wasting: A Metabolic Point of View

Rengin Elsurer Afsar; Baris Afsar; Talat Alp Ikizler

doi:10.1016/j.ekir.2023.04.027

Fibroblast Growth Factor 23 and Muscle Wasting: A Metabolic Point of View

Kidney Int Rep. 2023 May 3;8(7):1301-1314. doi: 10.1016/j.ekir.2023.04.027. eCollection 2023 Jul.

Authors

Rengin Elsurer Afsar^{1

2}, Baris Afsar^{1

2}, Talat Alp Ikizler^{1

3

4}

Affiliations

¹ Department of Medicine, Division of Nephrology and Hypertension, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
² Department of Nephrology, Suleyman Demirel University Faculty of Medicine, Isparta, Turkey.
³ Vanderbilt O'Brien Center for Kidney Disease, Nashville, Tennessee, USA.
⁴ Tennessee Valley Healthcare System, Nashville VA Medical Center, Nashville, Tennessee, USA.

Abstract

Protein energy wasting (PEW), mostly characterized by decreased body stores of protein and energy sources, particularly in the skeletal muscle compartment, is highly prevalent in patients with moderate to advanced chronic kidney disease (CKD). Fibroblast growth factor 23 (FGF23) is an endocrine hormone secreted from bone and has systemic actions on skeletal muscle. In CKD, FGF23 is elevated and its coreceptor α-klotho is suppressed. Multiple lines of evidence suggest that FGF23 is interconnected with various mechanisms of skeletal muscle wasting in CKD, including systemic and local inflammation, exaggerated oxidative stress, insulin resistance (IR), and abnormalities in adipocytokine metabolism. Investigation of metabolic actions of FGF23 on muscle tissue could provide new insights into metabolic and nutritional abnormalities observed in patients with CKD.

Keywords: adipokines; chronic kidney disease; fibroblast growth factor; inflammation; insulin resistance; muscle wasting; oxidative stress.

Publication types

Review