Exogenous　fibroblast　growth　factor　(FGF)　23　is　closely　associated　with　atrial　fibrillation　(AF)　and　is　able　to　alter　the　cardiac　electrophysiological　activity　by　increasing　intracellular　calcium.　While　its　arrhythmogenic　mechanism　remains　unclear,　this　study　aims　to　investigate　the　electrophysiological　effects　of　cardiac　FGF23　on　intracellular　calcium　in　atrial　cells　and　its　underlying　mechanism.　The　incidence　of　AF　was　significantly　decreased　in　FGF23(f/f)MyHC(Cre/+)　mice　compared　to　Cre　mice.　A　significant　increase　in　the　incidence　of　triggering　activity　(TA),　L-type　calcium　currents　(I-Ca,I-L)　and　systolic　calcium　transient　was　induced　in　neonatal　mice　atrial　myocytes　(NMAMs)　from　the　overexpression　of　FGF23.　Conversely,　the　opposite　effects　were　exhibited　as　a　reduced　diastolic　spontaneous　calcium　leak　and　weakened　Na+/Ca2+　exchange　(NCX)　function　in　cardiac　myocytes　from　FGF23(f/f)MyHCCre(/+)　mice,　which　can　reduce　incidences　of　AF　induced　by　delayed　after　depolarization　(DAD).　In　addition,　ryanodine-receptor　2　(RyR2)　of　calcium　regulatory　proteins　was　significantly　downregulated　in　FGF23(f/f)MyHC(Cre/+)　mice　and　upregulated　in　FGF23　overexpression　of　NMAMs.　In　conclusion,　overexpression　of　cardiac　FGF23　may　increase　the　susceptibility　to　AF　due　to　DAD　or　TA　induced　by　increasing　intracellular　calcium　in　atrial　myocytes.