Studies on Ang II signaling pathways in cardiomyocytes have identified key pathways contributing to HF progression, including redox-sensitive ERK1/2, p38, and NF-κB pathways driving Ang II-induced ROS production [47], ER stress triggered by excessive ROS [48], and activation of the NLRP3 inflammasome leading to elevated IL-1β and IL-18 levels [49]. This evidence concerns the gene IL18 and hydrops fetalis.