To analyse whether cardiac hypertrophy, alterations in CX43, and LV dysfunction in N1-Tg mice after I/R were due to unspecific upregulation of neuraminidase activity in the cardiomyocytes, a mouse with a cardiomyocyte-specific NEU3 overexpression (FVB/N-Tg(pRP.ExSi-TRENEU3; Tg(αMHC-tTA)) was generated. Here, NEU3 is linked to cardiac hypertrophy.