Toll-like receptors (TLR) are part of the innate immune system and bind pathogen associated patterns (PAMP) as well as damage associated patterns (DAMP). TLR4 deficiency (TLR4^-/-) has been shown to reduce pressure induced cardiac hypertrophy and ischemia reperfusion injury possibly due to reduced binding of DAMP. The influence of TLR2 and TLR9 on the development of cardiac hypertrophy has not yet been investigated, therefore TLR2^-/- and TLR9^-/- mice were exposed to transverse aortic constriction (TAC) to induce cardiac hypertrophy. Fourteen days after TAC surgery hemodynamic parameters were recorded by Millar pressure catheter. TAC surgery raised systolic arterial pressure 60-70 mmHg in WT and TLR2^-/- and TLR9^-/- mice. Also left ventricular systolic and end-diastolic pressure as well as dP/dt_max and dP/dt_min rose to the same extent in all genotypes. WT and TLR9^-/- did not differ in the degree of cardiac hypertrophy (left ventricular weight/body weight LVW/BW and LVW/tibia length LVW/TL) induced by TAC neither did both groups show differences in mRNA expression of inflammatory mediators (IL-1β and IL-6). Interestingly TLR2 deficiency increased cardiac hypertrophy in case of heart weight/body weight (HW/BW), HW/TL, and LVW/TL. The reason for this increased cardiac hypertrophy of TLR2^-/- mice has to be clarified by further investigations. Taken together both TLR2 and TLR9 affect cardiac hypertrophy in another way than TLR4.