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

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dc.creator Ikizler, Talat Alp
dc.creator Elsurer Afsar, Rengin
dc.creator Afsar, Baris
dc.date 2023-07-01T00:00:00Z
dc.date.accessioned 2025-02-25T10:23:51Z
dc.date.available 2025-02-25T10:23:51Z
dc.identifier 6c2b88db-5f25-4189-9cac-e6b59fa49f45
dc.identifier 10.1016/j.ekir.2023.04.027
dc.identifier https://avesis.sdu.edu.tr/publication/details/6c2b88db-5f25-4189-9cac-e6b59fa49f45/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/100066
dc.description 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.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title Fibroblast Growth Factor 23 and Muscle Wasting: A Metabolic Point of View
dc.type info:eu-repo/semantics/article


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