AGT and cardiac hypertrophy: Importantly, both AngII and aldosterone significantly up-regulate endogenous FGF23 expression in cardiac myocytes and induce hypertrophic cell growth, βMHC, ANP, and BNP. Whether these pathologies promoting cardiac hypertrophy and fibrosis are directly due to RAAS-mediated up-regulation of FGF23 in the heart or indirectly through the FGF23-mediated stimulation of RAAS is not clear.