Liu Shiyi, Zhang Ning
Department of Nephrology, Wangjing Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Ann Palliat Med. 2021 Dec;10(12):13002-13008. doi: 10.21037/apm-20-910. Epub 2021 Apr 9.
Vascular calcification (VC) has been proved the main pathophysiology basis that results in the cardiovascular disease which become the leading cause of death in patients with chronic kidney disease. The disordered mineral metabolism, hyperphosphatemia, overuse of calcium binders, occurred in the setting of uremia, have become the critical risk factors of vascular calcification in chronic kidney disease, in which the vascular smooth muscle cells undergo differentiation to osteoblast-like cells. The mechanisms involved in vascular calcification are complicated and exosomes, as novel players, are proven to play a vital role in VC and function as initializers for mineral deposition. Exosomal miRNAs play an important role in the regulation of cellular functions in vascular calcification. In this review, we focused on the roles of exosomes during VC, especially on their effects on regulating vascular calcification through initializing mineral deposition as a nidus, transporting microRNAs to the recipient cells and mediating the vascular smooth muscle cells differentiation to osteoblast-like cells.
血管钙化(VC)已被证明是导致心血管疾病的主要病理生理学基础,而心血管疾病是慢性肾脏病患者的主要死亡原因。在尿毒症背景下出现的矿物质代谢紊乱、高磷血症、钙结合剂的过度使用,已成为慢性肾脏病血管钙化的关键危险因素,其中血管平滑肌细胞会分化为成骨样细胞。血管钙化涉及的机制很复杂,而外泌体作为新的参与者,已被证明在VC中起重要作用,并作为矿物质沉积的起始因子发挥作用。外泌体微小RNA在血管钙化的细胞功能调节中起重要作用。在本综述中,我们重点关注外泌体在VC过程中的作用,特别是它们通过作为矿化核心起始矿物质沉积、将微小RNA转运到受体细胞以及介导血管平滑肌细胞向成骨样细胞分化来调节血管钙化的作用。
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