Furthermore, it has been shown that TRPV1-mediated Ca2+ signals recruit cardioprotective signaling pathways in several mouse models of AMI and HF [171,172,173], whereas the genetic deletion of TRPV1 exacerbated cardiac hypertrophy, myocardial inflammation and fibrosis in a mouse model of TAC [160]. The gene discussed is TRPV1; the disease is hydrops fetalis.