C-type natriuretic peptide (CNP)

C-type natriuretic peptide (CNP), encoded by the NPPC gene, is a member of the natriuretic peptide family which also includes atrial (ANP) and B-type (BNP) natriuretic peptides[1][2]. Unlike ANP and BNP, which primarily act in natriuresis and diuresis, CNP is an endothelium-derived ligand regulating vascular homeostasis, local blood flow, and systemic blood pressure, as well as long bone growth[2][3]. CNP acts chiefly through natriuretic peptide receptor-B (NPR-B), stimulating guanylyl cyclase activity and increasing intracellular cGMP, and also through natriuretic peptide receptor-C (NPR-C), mediating clearance and additional cardioprotective effects[2][3]. It plays a critical role in cardiovascular health, protecting against fibrosis and hypertrophy, and maintaining myocardial function during injury[3]. CNP is under investigation as a therapeutic target, especially for cardiovascular disease, although no clinical drugs currently target CNP directly. Therapeutic challenges involve precise modulation of its systemic effects to avoid adverse outcomes such as hypotension or abnormal cardiac/bone growth[2][3][1].

Other names

C-type natriuretic peptidenatriuretic peptide precursor type CNPPCCNP-22CNP-29CNP-53CNP2CNP

Activation of NPR-B (guanylyl cyclase-coupled receptor): increases cGMP, leading to vasorelaxation and inhibition of fibroblast proliferation. Activation of NPR-C (clearance receptor, and possibly GPCR signaling): mediates cardioprotective effects, modifies leukocyte/platelet activity, and contributes to antifibrotic, anti-hypertrophic responses.