Both Nod1 deficient and RIP2 deficient mice are protected from TAC-mediated left ventricular pressure overload-induced cardiac hypertrophy and cardiac dysfunction as evidenced by decreased heart weight and hypertrophic marker genes ANP and BNP, decreased perivascular and interstitial fibrosis, improved left ventricle end-diastolic dimension and fractional shortening compared to that of post-TAC wildtype mice. Here, NPPA is linked to cardiac hypertrophy.