Heart valve

Heart valves are specialized anatomical structures within the heart—comprising the aortic, mitral, tricuspid, and pulmonary valves—that ensure unidirectional blood flow by opening and closing in response to pressure gradients during the cardiac cycle (StatPearls, NBK532265). They are composed of an extracellular matrix-rich leaflet tissue populated by valvular interstitial cells (VICs) and covered by a layer of valvular endothelial cells (VECs). While heart valves are not molecular targets in the traditional sense (such as a specific receptor or enzyme), they are the primary site of significant pathologies including calcific aortic valve disease (CAVD), stenosis, and regurgitation, which can lead to heart failure (NIH, Valvular Heart Disease). Pharmacologically, heart valves are most notable for their susceptibility to drug-induced valvulopathy, where certain medications act as off-target agonists of the serotonin 5-HT2B receptor on VICs, leading to pathological remodeling and fibrosis (JACC, 15610751). Currently, there are no approved pharmacological therapies to reverse structural valve degradation, making surgical repair or transcatheter replacement the standard of care for advanced disease.

Other names

Cardiac valveAtrioventricular valveSemilunar valveAortic valveMitral valveTricuspid valvePulmonary valve

Heart valves are not molecular targets; however, drugs that interact with them typically do so via off-target agonism of the serotonin 5-HT2B receptor located on valvular interstitial cells, which triggers overgrowth and fibrosis (JACC, 15610751).