Ask about this productRelated genes to: FGF23 protein
- Gene:
- FGF23 NIH gene
- Name:
- fibroblast growth factor 23
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 12p13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2000-05-16
- Date modifiied:
- 2016-10-05
Related products to: FGF23 protein
Related articles to: FGF23 protein
- Elevated phosphate concentration in proximal tubular fluid promotes calcium phosphate microcrystallopathy, thereby accelerating the progression of chronic kidney disease (CKD). However, the clinical significance of proximal tubular phosphate exposure in humans remains uncertain. We aimed to determine whether estimated proximal tubular fluid phosphate concentration (ePTFp) is independently associated with age-related kidney function decline in adults with and without CKD. - Source: PubMed
Publication date: 2026/03/16
Kosaki KeiseiMori ShoyaMatsui MasahiroYoshioka MasakiPark JiyeonNishitani NatsumiYoshikoshi ShunMurasaki WataruSaito ChieGosho MasahikoMaeda SeijiKuro-O MakotoYamagata Kunihiro - X-linked hypophosphatemia (XLH), primarily caused by mutations of the gene, is the most common cause of genetic rickets. Pediatric cases of XLH typically present with elevated levels of serum fibroblast growth factor 23 (FGF23), hypophosphatemia, rickets, and impaired growth. Here, we report a 2-year-old boy diagnosed with XLH, presenting with short stature, genu varum, and hypophosphatemia. Sanger sequencing revealed a novel mutation of the gene, comprising a 62-bp poly-T and a 421-bp long interspersed element-1 (LINE-1) insertion into exon 22, which appears to induce the hypophosphatemia. This study presents the first documented case of XLH associated with a partial LINE-1 insertion in . We suggest that LINE-1 transposon element insertions be considered in XLH patients lacking other known mutations. - Source: PubMed
Publication date: 2026/04/30
Li DongmeiPeng WanKang LuGeng JiaLu YuLu Jing - Tumor-induced osteomalacia (TIO) is a rare paraneoplastic syndrome resulting from excessive secretion of fibroblast growth factor-23 (FGF23) by phosphaturic mesenchymal tumors (PMTs). We report the case of a 35-year-old man with a three-year history of progressive musculoskeletal symptoms and severe mobility impairment, who had not received a correct diagnosis during this period. Laboratory evaluation revealed severe hypophosphatemia and elevated FGF23 levels. Magnetic resonance imaging (MRI) and Ga-DOTA-TATE PET/CT identified a metabolically active lesion in the sartorius muscle. Surgical resection of the tumor resulted in complete resolution of symptoms, restoration of mobility and normalization of phosphate metabolism. This case emphasizes the importance of considering TIO in patients with unexplained osteomalacia and highlights the diagnostic value of functional imaging. - Source: PubMed
Publication date: 2026/04/17
Rymon Lipinska WeronikaFilckowska NataliaEkman MarcinKobiela Jarosław - Steroid-induced osteonecrosis of the femoral head (SONFH) is a terrible side effect of glucocorticoid therapy that causes problems with microvascular integrity, lipid metabolism, and a range of programmed cell death pathways. Recent studies have shown that autophagy can have different effects on osteoblasts and endothelial cells depending on the situation. These effects are mediated by the AMPK/mTOR, PINK1/Parkin, SIRT1/FoxO1, and PI3K/Akt/mTOR pathways. At the same time, apoptosis is caused by lowering Wnt/β-catenin, raising STAT1/caspase-3, and throwing off the balance of the OPG/RANKL/RANK axis. This makes it harder for bones to develop and makes osteoclasts work too hard. The growing contributions of ferroptosis (SLC7A11/GPX4 axis), necroptosis (RIPK1/RIPK3/MLKL), oxidative stress (NOX-JNK-c-Jun and Keap1-Nrf2), and pyroptosis (NLRP3/Caspase-1 and Caspase-4/5/11 inflammasomes) show that there is a complex network of cell death that makes SONFH worse. Preclinical treatments such as rapamycin, puerarin, lithium, NAC, necrostatin-1, luteolin, MCC950, antler peptides, and FGF23 inhibitors show promise in working together to change these pathways. A better knowledge of pathway crosstalk and dosage-dependent effects is the first step toward tailored, multi-modal therapeutics that can stop and treat SONFH. This review article looks at the signalling pathways that are currently thought to be involved in the pathogenesis of SONFH. Its goal is to help people better understand the disease and how to avoid and treat it more effectively. - Source: PubMed
Publication date: 2026/04/30
Niu XiaojuanLi JunYan ZhongshengChen TiantianYan XiangyongWang JianChen Guangyan - Fibroblast growth factor 23 (FGF23) is an endocrine regulator of phosphate homeostasis produced by bone. This review aims to examine the role of FGF23 in bone biology, with a focus on its contributions to skeletal abnormalities in hereditary hypophosphatemia and chronic kidney disease (CKD). - Source: PubMed
Publication date: 2026/04/30
Kentrup DominikMartin Aline