Introduction to Our Research Paper Writing Services

Calcific Aortic Valve Disease (CAVD) is a progressive cardiovascular condition, evolving from early sclerosis to severe stenosis, impacting heart valve function and increasing risks of cardiovascular mortality. This empirical review explores animal models pivotal for understanding CAVD’s pathobiology, highlighting its active, cell-mediated processes rather than passive degeneration. As the third most common heart disease after coronary artery disease and hypertension, CAVD shares risk factors like high cholesterol, diabetes, and aging, yet diverges from atherosclerosis, with approximately 50% of patients lacking severe atherosclerotic lesions. Mouse, rabbit, and porcine models, including genetically modified strains like LDLR-deficient mice and Watanabe rabbits, replicate human CAVD features such as calcification, fibrosis, and inflammation. These models, supported by high-fat diets and genetic mutations, offer insights into molecular mechanisms, including Notch signaling and endothelial dysfunction, driving valve thickening and calcium deposition. By examining early sclerosis and advanced stenosis, this review underscores the translational potential of animal models for developing novel therapies, enhancing diagnosis, and preventing CAVD progression, addressing a critical need in cardiovascular research.