Progressive decline in circulating CNP with aging is associated with progressive cardiac fibrosis and myocardial impairment

Background Cardiac aging is associated with altered myocardial structure and function that may contribute to the development of heart failure (HF), particularly in the elderly. C-type natriuretic peptide (CNP) is of endothelial cell origin and represents the most potent anti-fibrotic peptide of the natriuretic peptide (NP) family. CNP activates the NP receptor-B (NPR-B), which is found in high abundance in cardiac fibroblasts. Further, selective cardiac knockout of NPR-B contributes to exaggerated cardiomyocyte hypertrophy in response to pressure overload. In addition, infusion of CNP suppresses post-myocardial infarction (MI) induced cardiac fibrosis in a rodent model of MI. The impact of aging on circulating CNP and associated left ventricular (LV) structure and function are undefined.