GNAQ and hydrops fetalis: GPCRs like the Ang II receptor type 1, endothelin receptors, and α1-adrenergic receptors are activated by hormones like Ang II, leading to downstream signaling involving proteins such as phospholipase C and MAPKs.[34] Studies show that manipulating GPCR signaling can influence heart growth, with overexpression of Gαq causing HF and reduced signaling leading to less hypertrophy.[91–93] Current therapies targeting GPCR pathways include ACE inhibitors and β-blockers.