Oxidative stress and valvular endothelial cells in aortic valve calcification

Calcified aortic valve disease (CAVD) is a common cardiovascular disease in elderly individuals. Although it was previously considered a degenerative disease, it is, in fact, a progressive disease involving multiple mechanisms. Aortic valve endothelial cells, which cover the outermost layer of the aortic valve and are directly exposed to various pathogenic factors, play a significant role in the onset and progression of CAVD. Hemodynamic changes can directly damage the structure and function of valvular endothelial cells (VECs). This leads to inflammatory infiltration and oxidative stress, which promote the progression of CAVD. VECs can regulate the pathological differentiation of valvular interstitial cells (VICs) through NO and thus affect the process of CAVD. Under the influence of pathological factors, VECs can also be transformed into VICs through EndMT, and then the path-ological differentiation of VICs eventually leads to the formation of calcification. This review discusses the role of VECs, especially the role of oxidative stress in VECs, in the process of aortic valve calcification.

Automated summary

Calcified aortic valve disease (CAVD) is a progressive cardiovascular disease involving multiple mechanisms, rather than simply a degenerative disease. Aortic valve endothelial cells (VECs), which are directly exposed to pathogenic factors, play a significant role in the onset and progression of CAVD. Hemodynamic changes damage VECs, leading to inflammatory infiltration and oxidative stress, promoting CAVD progression. VECs also regulate the pathological differentiation of valvular interstitial cells (VICs) and eventually lead to calcification.