Molecular and cellular mechanisms of aortic stenosis

摘要: Calcific aortic stenosis is the most common cause of valve replacement in developed countries, and this condition increases prevalence with advancing age. The fibrotic thickening calcification are eventual endpoint both non-rheumatic calcific rheumatic stenoses. New observations human valves support hypothesis that degenerative valvular result active bone formation valve, which may be mediated through a process osteoblast-like differentiation these tissues. Additionally histopathologic evidence suggests early lesions not just disease secondary to aging, but an cellular follows classical "response injury hypothesis" similar situation atherosclerosis. Although there similarities risk factor as well atherogenesis, all patients coronary artery or atherosclerosis have stenosis. This review mainly focuses on potential vascular molecular mechanisms involved pathogenesis Namely extracellular matrix remodeling, angiogenesis, inflammation, eventually resulting been shown play role Several mediators related underlying mechanisms, including growth factors especially transforming factor-beta1 endothelial factors, cathepsin enzymes, adhesion molecules, regulatory proteins metalloproteinases demonstrated, however target attacked defined yet.