Division of Nephrology, Department of Medicine, Cardinal-Tien Hospital, New Taipei City 231, Taiwan.
School of Medicine, Fu-Jen Catholic University, New Taipei City 234, Taiwan.
Int J Mol Sci. 2020 Apr 2;21(7):2466. doi: 10.3390/ijms21072466.
Vascular calcification, which involves the deposition of calcifying particles within the arterial wall, is mediated by atherosclerosis, vascular smooth muscle cell osteoblastic changes, adventitial mesenchymal stem cell osteoblastic differentiation, and insufficiency of the calcification inhibitors. Recent observations implied a role for mesenchymal stem cells and endothelial progenitor cells in vascular calcification. Mesenchymal stem cells reside in the bone marrow and the adventitial layer of arteries. Endothelial progenitor cells that originate from the bone marrow are an important mechanism for repairing injured endothelial cells. Mesenchymal stem cells may differentiate osteogenically by inflammation or by specific stimuli, which can activate calcification. However, the bioactive substances secreted from mesenchymal stem cells have been shown to mitigate vascular calcification by suppressing inflammation, bone morphogenetic protein 2, and the Wingless-INT signal. Vitamin D deficiency may contribute to vascular calcification. Vitamin D supplement has been used to modulate the osteoblastic differentiation of mesenchymal stem cells and to lessen vascular injury by stimulating adhesion and migration of endothelial progenitor cells. This narrative review clarifies the role of mesenchymal stem cells and the possible role of vitamin D in the mechanisms of vascular calcification.
血管钙化涉及到钙盐在动脉壁内的沉积，是动脉粥样硬化、血管平滑肌细胞成骨样改变、血管外膜间充质干细胞成骨样分化以及钙化抑制剂不足等多种因素共同作用的结果。最近的研究观察提示间充质干细胞和内皮祖细胞在血管钙化中起作用。间充质干细胞位于骨髓和动脉外膜层。内皮祖细胞起源于骨髓，是修复受损内皮细胞的重要机制。间充质干细胞可通过炎症或特定刺激向成骨样分化，从而激活钙化。然而，间充质干细胞分泌的生物活性物质通过抑制炎症、骨形态发生蛋白 2 和 Wingless-INT 信号来减轻血管钙化。维生素 D 缺乏可能导致血管钙化。维生素 D 补充已被用于调节间充质干细胞的成骨样分化，并通过刺激内皮祖细胞的黏附和迁移来减轻血管损伤。本综述阐明了间充质干细胞的作用以及维生素 D 在血管钙化机制中的可能作用。
