CNP (C-type natriuretic peptide) is an endogenous peptide hormone that functions as a key regulator of vascular homeostasis and bone metabolism. The gene encodes a 126-residue precursor that is processed into bioactive peptides, primarily CNP-22 and CNP-53 1. CNP signals through the guanylyl cyclase B (GC-B) receptor to activate the cGMP-dependent pathway 2, mediating multiple protective effects: (1) vascular protection through endothelium-dependent vasodilation via NPRB-mediated cGMP production in vascular smooth muscle cells 3; (2) anti-inflammatory macrophage polarization and atherosclerotic plaque stabilization through HIF-1α degradation 4; (3) bone formation promotion by antagonizing FGF-23/MAPK signaling in chr17 kidney disease 5; and (4) attenuation of pericyte dysfunction in pulmonary arterial hypertension through FoxO3 transcription factor activation 2. CNP also regulates oocyte maturation through cGMP modulation 6. Therapeutically, enhancing CNP bioactivity via drugs like LCZ696 shows promise for treating atherosclerosis and heart failure. Mutations cause hypomyelinating leukodystrophy 20, indicating roles in neural development beyond its vascular functions.