Endothelial-to-Mesenchymal Transition in Calcific Aortic Valve Disease.
Xiaochun Ma, Diming Zhao, Peidong Yuan, Jinzhang Li, Yan Yun, Yuqi Cui, Tao Zhang, Jiwei Ma, Liangong Sun, Huibo Ma, Yuman Zhang, Haizhou Zhang, Wenlong Zhang, Junjie Huang, Chengwei Zou, Zhengjun Wang
Abstract
Nevertheless, pharmaceutical trials that attempted to target inflammation and dyslipidemia have produced disappointing results in CAVD. While senescence is a well-documented risk factor, the sophisticated regulatory networks have not been adequately explored underlying the aberrant calcification and osteogenesis in CAVD. Valvular endothelial cells (VECs), a type of resident effector cells in aortic leaflets, are crucial in maintaining valvular integrity and homeostasis, and dysfunctional VECs are a major contributor to disease initiation and progression. Accumulating evidence suggests that VECs undergo a phenotypic and functional transition to mesenchymal or fibroblast-like cells in CAVD, a process known as the endothelial-to-mesenchymal transition (EndMT) process. The relevance of this transition in CAVD has recently drawn great interest due to its importance in both valve genesis at an embryonic stage and CAVD development at an adult stage. Hence EndMT might be a valuable diagnostic and therapeutic target for disease prevention and treatment. This mini-review summarized the relevant literature that delineates the EndMT process and the underlying regulatory networks involved in CAVD.