Background: FGF23 plays an important role in calcium-phosphorus metabolism. Other roles of FGF23 have recently been reported, such as commitment to myocardium enlargement and immunological roles in the spleen. In this study, we aimed to identify the roles of FGF23 in the kidneys other than calcium-phosphorus metabolism.
Methods: DNA microarrays and bioinformatics tools were used to analyze gene expression in mIMCD3 mouse renal tubule cells following treatment with FGF23, erythropoietin and/or an inhibitor of ERK.
Results: Three protein-coding genes were upregulated and 12 were downregulated in response to FGF23. Following bioinformatics analysis of these genes, PPARγ and STAT3 were identified as candidate transcript factors for mediating their upregulation, and STAT1 as a candidate for mediating their downregulation. Because STAT1 and STAT3 also mediate erythropoietin signaling, we investigated whether FGF23 and erythropoietin might show interactive effects in these cells. Of the 15 genes regulated by FGF23, 11 were upregulated by erythropoietin; 10 of these were downregulated following cotreatment with FGF23. Inhibition of ERK, an intracellular mediator of FGF23, reversed the effects of FGF23. However, FGF23 did not influence STAT1 phosphorylation, suggesting that it impinges on erythropoietin signaling through other mechanisms.
Conclusion: Our results suggest cross talk between erythropoietin and FGF23 signaling in the regulation of renal epithelial cells.
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http://dx.doi.org/10.2147/IJNRD.S158422 | DOI Listing |
World J Diabetes
January 2025
Department of Endocrinology, Wuhu Second People's Hospital, Wuhu 241000, Anhui Province, China.
Background: The progression of diabetic kidney disease (DKD) affects the patient's kidney glomeruli and tubules, whose normal functioning is essential for maintaining normal calcium (Ca) and phosphorus (P) metabolism in the body. The risk of developing osteoporosis (OP) in patients with DKD increases with the aggravation of the disease, including a higher risk of fractures, which not only affects the quality of life of patients but also increases the risk of death.
Aim: To analyze the risk factors for the development of OP in patients with DKD and their correlation with Ca-P metabolic indices, fibroblast growth factor 23 (FGF23), and Klotho.
J Clin Endocrinol Metab
January 2025
Kidney Research Institute, Department of Medicine, University of Washington, Seattle, WA.
Context: The response to treatment with vitamin D varies between patients.
Objective: To identify genetic variants associated with the biochemical response to vitamin D3 supplementation.
Design: Randomized placebo-controlled trial conducted between 2017 and 2019.
Nat Rev Nephrol
January 2025
APHP, Reference Center for Rare Diseases of Calcium and Phosphate Metabolism, and Filière OSCAR, endo ERN and ERN BOND, Paris, France.
X-linked hypophosphataemia (XLH) is a rare metabolic bone disorder caused by pathogenic variants in the PHEX gene, which is predominantly expressed in osteoblasts, osteocytes and odontoblasts. XLH is characterized by increased synthesis of the bone-derived phosphaturic hormone fibroblast growth factor 23 (FGF23), which results in renal phosphate wasting with consecutive hypophosphataemia, rickets, osteomalacia, disproportionate short stature, oral manifestations, pseudofractures, craniosynostosis, enthesopathies and osteoarthritis. Patients with XLH should be provided with multidisciplinary care organized by a metabolic bone expert.
View Article and Find Full Text PDFInt J Cardiol Heart Vasc
February 2025
Department of Nephropathy, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Background: Heart failure (HF) is a significant cause of death among patients with chronic kidney disease (CKD). Emerging data suggest a crucial role of fibroblast growth factor 23 (FGF23) in the pathogenesis of HF in CKD patients. The present study aimed to investigate whether the serum intact FGF23 (iFGF23) level is elevated when ejection fraction (EF) is preserved and to evaluate its predictive value for incident HF and cardiac mortality in CKD patients with preserved EF.
View Article and Find Full Text PDFJ Orthop Case Rep
January 2025
Department of Orthopaedic Surgery, Maulana Azad Medical College, Bahadur Shah Marg, New Delhi, India.
Introduction: Tumoral calcinosis is a rare hereditary condition characterized by the deposition of calcium phosphate and hydroxyapatite in periarticular soft tissues. First described by Giard and Duret in 1898 and later detailed by Inclan in 1943, this condition has often been confused with other forms of periarticular calcification. Tumoral calcinosis predominantly affects young males and is typically found around major joints, such as the shoulder, elbow, hip, ankle, and wrist.
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