Osteoporosis is a public health concern associated with an increased risk of bone fractures and vascular calcification. Vitamin K presents unique benefits on these issues, although understudied. The two main forms of vitamin K are phylloquinone (vitamin K₁) and menaquinone (vitamin K₂). In this study, it was especially investigated the action of vitamin K₂ in bones and vessels. Vitamin K₂ has shown to stimulate bone formation by promoting osteoblast differentiation and carboxylation of osteocalcin, and increasing alkaline phosphatase, insulin-like growth factor-1, growth differentiation factor-15, and stanniocalcin 2 levels. Furthermore, vitamin K₂ reduces the pro-apoptotic proteins Fas and Bax in osteoblasts, and decreases osteoclast differentiation by increasing osteoprotegerin and reducing the receptor activator of nuclear factor kappa-B ligand. In blood vessels, vitamin K₂ reduces the formation of hydroxyapatite, through the carboxylation of matrix Gla protein and Gla rich protein, inhibits the apoptosis of vascular smooth muscle cells, by increasing growth arrest-specific gene 6, and reduces the transdifferentiation of vascular smooth muscle cells to osteoblasts. The commonly used dosage of vitamin K₂ in human studies is 45 mg/day and its application can be an interesting strategy in benefitting bone and vascular health, especially to osteoporotic post-menopausal women.

骨质疏松症是公共卫生问题，与骨折和血管钙化的风险增加有关。维生素K在这些问题上显示出独特的益处，尽管未被充分研究。维生素K的两种主要形式是叶醌（维生素K ₁）和甲萘醌（维生素K ₂）。在这项研究中，特别研究了维生素K ₂在骨骼和血管中的作用。维生素K ₂已显示出通过促进成骨细胞的分化和骨钙素的羧化并增加碱性磷酸酶，胰岛素样生长因子-1，生长分化因子15和斯坦钙素2的水平来刺激骨形成。此外，维生素K ₂减少成骨细胞中促凋亡蛋白Fas和Bax，并通过增加骨保护素和减少核因子kappa-B配体的受体活化剂来减少破骨细胞分化。在血管中，维生素K ₂通过基质Gla蛋白和富Gla蛋白的羧化作用减少羟基磷灰石的形成，通过增加生长停滞特异性基因6抑制血管平滑肌细胞的凋亡，并减少血管平滑肌的转分化作用肌细胞到成骨细胞。在人体研究中，维生素K ₂的常用剂量为45毫克/天，其应用可能是有益于骨骼和血管健康的有趣策略，尤其是对于绝经后骨质疏松的妇女。