Interestingly, TAC-induced cardiac remodeling and dysfunction observed in PDE1C wild-type (PDE1C-WT) mice was significantly alleviated in PDE1C-KO mice, as indicated by reduced chamber dilation, myocardial hypertrophy, cardiac myocyte apoptosis, and interstitial fibrosis, as well as attenuated loss of fractional shortening and ejection fraction [49]. Here, PDE1C is linked to cardiac hypertrophy.