{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Faul C"],"funding":["NIDDK NIH HHS","NCRR NIH HHS","NIA NIH HHS"],"pagination":["4393-408"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3204831"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["121(11)"],"pubmed_abstract":["Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or in"],"journal":["The Journal of clinical investigation"],"pubmed_title":["FGF23 induces left ventricular hypertrophy."],"pmcid":["PMC3204831"],"funding_grant_id":["U01 DK061021","RR05096","U01 DK060990","5U01DK060984","5U01DK060963","R01 DK081374","5U01DK060902","U01 DK061028","UL1 RR029879","K24 DK062234","K23DK087858","M01 RR-000042","K23DK081673","R01 DK091218","F30DK091057","M01 RR016500","UL1 RR025005","R01DK081374","U01 DK060902","UL1 RR024134","M01 RR16500","K23 DK081673","R01DK091392","UL1 RR024131","5U01DK061028","R01AG019712","K23 DK087858","P30DK-07938","U01 DK060963","U01 DK060984","R01 DK076116","R01DK076116","U01 DK060980","5U01DK06102","UL1 RR024989","R01 DK092461","F30 DK091057","R01 AG019712","5U01DK60980","R01 DK091392","UL1 RR024986","R01 DK062472","M01 RR005096","5U01DK061021","RR024131","5U01DK060990","M01 RR000042"],"pubmed_authors":["Tiemann K","Hu MC","Soliman EZ","Hill JA","Isakova T","Mundel P","Keane MG","Morales A","Kusek JW","Lincoln J","Go AS","Feldman HI","Townsend RR","Faul C","Oskouei B","St John Sutton M","Wolf M","Kuro-O M","Sloan A","Scialla J","Chen J","Amaral AP","Moe OW","Hare JM","Gadegbeku C","Di Marco GS","Kentrup D","Aguillon-Prada R","Gutierrez OM","Rosas SE","Fischer M","Nessel L","Brand M","Reuter S","Ojo A"],"additional_accession":[]},"is_claimable":false,"name":"FGF23 induces left ventricular hypertrophy.","description":"Chronic kidney disease (CKD) is a public health epidemic that increases risk of death due to cardiovascular disease. Left ventricular hypertrophy (LVH) is an important mechanism of cardiovascular disease in individuals with CKD. Elevated levels of FGF23 have been linked to greater risks of LVH and mortality in patients with CKD, but whether these risks represent causal effects of FGF23 is unknown. Here, we report that elevated FGF23 levels are independently associated with LVH in a large, racially diverse CKD cohort. FGF23 caused pathological hypertrophy of isolated rat cardiomyocytes via FGF receptor-dependent activation of the calcineurin-NFAT signaling pathway, but this effect was independent of klotho, the coreceptor for FGF23 in the kidney and parathyroid glands. Intramyocardial or in","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Nov","modification":"2026-04-13T08:40:00.804Z","creation":"2019-03-27T00:45:31Z"},"accession":"S-EPMC3204831","cross_references":{"pubmed":["21985788"],"doi":["10.1172/jci46122","10.1172/JCI46122"]}}