Qin Zheng, Liao Ruoxi, Xiong Yuqin, Jiang Luojia, Li Jiameng, Wang Liya, Han Mei, Sun Si, Geng Jiwen, Yang Qinbo, Zhang Zhuyun, Li Yupei, Du Heyue, Su Baihai
Department of nephrology and National Clinical Research Center for Geriatrics, West China Hospital of Sichuan University, Chengdu, China.
Institute for Disaster Management and Reconstruction, Sichuan University, Chengdu, China.
Ann Transl Med. 2021 Apr;9(7):579. doi: 10.21037/atm-20-7355.
Vascular calcification (VC) is the abnormal deposition of calcium, phosphorus, and other minerals in the vessel wall and can be commonly observed in diabetes, chronic kidney disease, and chronic inflammatory disease. It is closely associated with mortality from cardiovascular events. Traditionally, calcification is considered as a degenerative disease associated with the aging process, while increasing evidence has shown that the occurrence and development of calcification is an active biological process, which is highly regulated by multiple factors. The molecular mechanisms of VC have not yet been fully elucidated. Exosomes, as important transporters of substance transport and intercellular communication, have been shown to participate in VC. The regulation of VC by exosomes involves a number of complex biological processes, which occur through a variety of interaction mechanisms. However, the specific role and mechanism of exosomes in the process of VC are still not fully understood and require further study. This review will briefly describe the roles of exosomes in the process of VC including in the promotion of extracellular mineral deposits, induction of phenotypic conversion of vascular smooth muscle cells (VSMCs), transport of microRNA between cells, and regulation on autophagy and oxidative stress, with the aim of providing novel ideas for the clinical diagnosis and treatment of VC.
血管钙化（VC）是钙、磷和其他矿物质在血管壁的异常沉积，常见于糖尿病、慢性肾病和慢性炎症性疾病中。它与心血管事件导致的死亡率密切相关。传统上，钙化被认为是一种与衰老过程相关的退行性疾病，然而越来越多的证据表明，钙化的发生和发展是一个活跃的生物学过程，受到多种因素的高度调控。VC的分子机制尚未完全阐明。外泌体作为物质运输和细胞间通讯的重要载体，已被证明参与了VC过程。外泌体对VC的调控涉及许多复杂的生物学过程，通过多种相互作用机制发生。然而，外泌体在VC过程中的具体作用和机制仍未完全了解，需要进一步研究。本综述将简要描述外泌体在VC过程中的作用，包括促进细胞外矿物质沉积、诱导血管平滑肌细胞（VSMC）表型转化、细胞间微小RNA的运输以及对自噬和氧化应激的调控，旨在为VC的临床诊断和治疗提供新思路。
