Abstract
Calcific aortic valve disease (CAVD) is a prevalent condition characterized by pathological thickening and calcification of the aortic valve, leading to increased pressure overload and cardiac remodeling, particularly in individuals aged 65 and older. This review synthesizes recent advances in understanding the pathogenesis of CAVD, focusing on key mechanisms including hemodynamic alterations, endothelial dysfunction, lipid deposition, inflammation, and fibrotic calcification. We evaluate emerging therapeutic targets based on pivotal basic research and clinical trials, highlighting the potential for mechanism-oriented interventions. Furthermore, we explore the implications of lipid-lowering therapies, anti-inflammatory strategies, and antifibrocalcific agents, as well as novel bioprosthetic designs aimed at enhancing patient outcomes. Additionally, we discuss the inherent genetic and molecular backgrounds influencing individual susceptibility to CAVD, emphasizing the promise of personalized therapy. By bridging the gap between basic science and clinical application, this review aims to guide future research efforts toward more effective prevention and treatment strategies for CAVD.