Increased activity of Gαq/PLC-β, by generating diacylglycerol that can activate PKC activity, likely plays a role in promoting Nox2-dependent superoxide production in VH/HF; in addition, activated mineralocorticoid receptors are known to stimulate Nox2-dependent superoxide production in the heart via a non-genomic mechanism [85,86,87]. Here, GNAQ is linked to hydrops fetalis.