{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Czaya B"],"funding":["NIDCR NIH HHS","NIDDK NIH HHS","NHLBI NIH HHS","National Institutes of Health"],"pagination":["e74782"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8963881"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["11"],"pubmed_abstract":["Elevations in plasma phosphate concentrations (hyperphosphatemia) occur in chronic kidney disease (CKD), in certain genetic disorders, and following the intake of a phosphate-rich diet. Whether hyperphosphatemia and/or associated changes in metabolic regulators, including elevations of fibroblast growth factor 23 (FGF23) directly contribute to specific complications of CKD is uncertain. Here, we report that similar to patients with CKD, mice with adenine-induced CKD develop inflammation, anemia, and skeletal muscle wasting. These complications are also observed in mice fed high phosphate diet even without CKD. Ablation of pathologic FGF23-FGFR4 signaling did not protect mice on an increased phosphate diet or mice with adenine-induced CKD from these sequelae. However, low phosphate diet ame"],"journal":["eLife"],"pubmed_title":["Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signaling."],"pmcid":["PMC8963881"],"funding_grant_id":["K08 DK111980","R01-HL-145528","T90 DE022736","R01 DK125459","R01-HL-128714","F31 DK115074","F31 DK117550","K24 DK116180","F31-DK-117550","F31-DK-115074","R01-DK-125459","R01 HL145528","R01 DK087727","R01 HL128714"],"pubmed_authors":["Kentrup D","Jung G","Salusky IB","Babitt JL","Westbrook D","Czaya B","Faul C","Gutierrez O","Campos I","Heitman K","Hanudel M","Yanucil C"],"additional_accession":[]},"is_claimable":false,"name":"Hyperphosphatemia increases inflammation to exacerbate anemia and skeletal muscle wasting independently of FGF23-FGFR4 signaling.","description":"Elevations in plasma phosphate concentrations (hyperphosphatemia) occur in chronic kidney disease (CKD), in certain genetic disorders, and following the intake of a phosphate-rich diet. Whether hyperphosphatemia and/or associated changes in metabolic regulators, including elevations of fibroblast growth factor 23 (FGF23) directly contribute to specific complications of CKD is uncertain. Here, we report that similar to patients with CKD, mice with adenine-induced CKD develop inflammation, anemia, and skeletal muscle wasting. These complications are also observed in mice fed high phosphate diet even without CKD. Ablation of pathologic FGF23-FGFR4 signaling did not protect mice on an increased phosphate diet or mice with adenine-induced CKD from these sequelae. However, low phosphate diet ame","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Mar","modification":"2025-06-01T02:36:55.831Z","creation":"2025-06-01T02:36:55.831Z"},"accession":"S-EPMC8963881","cross_references":{"pubmed":["35302487"],"doi":["10.7554/eLife.74782"]}}