Skeletal muscle-specific musclin overexpression in one study demonstrated its inhibition of cardiac fibrosis and dysfunction and improvement of ventricular contractility during chronic pressure overload via competitively bonding to the natriuretic peptide receptors C (NPRC) and increasing the C-type natriuretic peptide (CNP)/natriuretic peptide receptor B (NPR-B) signaling, while musclin knockout aggravated the advancement of HF. Here, NPR3 is linked to hydrops fetalis.