PDF(Pubmed)
Abstract：
Magnesium (Mg), a nutritional element which is essential for bone development and mineralization, has a role in the progression of osteoporosis. Osteoporosis is a multifactorial disease characterized by significant deterioration of bone microstructure and bone loss. Mg deficiency can affect bone structure in an indirect way through the two main regulators of calcium homeostasis (parathyroid hormone and vitamin D). In human osteoblasts (OBs), parathyroid hormone regulates the expression of receptor activator of nuclear factor-κ B ligand (RANKL) and osteoprotegerin (OPG) to affect osteoclast (OC) formation. In addition, Mg may also affect the vitamin D3 -mediated bone remodeling activity. vitamin D3 usually coordinates the activation of the OB and OC. The unbalanced activation OC leads to bone resorption. The RANK/RANKL/OPG axis is considered to be a key factor in the molecular mechanism of osteoporosis. Mg participates in the pathogenesis of osteoporosis by affecting the regulation of parathyroid hormone and vitamin D levels to affect the RANK/RANKL/OPG axis. Different factors affecting the axis and enhancing OC function led to bone loss and bone tissue microstructure damage, which leads to the occurrence of osteoporosis. Clinical research has shown that Mg supplementation can alleviate the symptoms of osteoporosis to some extent.
摘要：
镁(Mg),一种对骨骼发育和矿化至关重要的营养元素，在骨质疏松症的进展中起作用。骨质疏松症是一种多因素疾病，其特征是骨微结构和骨丢失的显着恶化。镁缺乏可以通过钙稳态的两个主要调节剂（甲状旁腺激素和维生素D）间接影响骨骼结构。在人类成骨细胞（OBs）中，甲状旁腺激素通过调节核因子-κB受体活化因子配体(RANKL)和骨保护素(OPG)的表达影响破骨细胞(OC)的形成。此外,Mg还可能影响维生素D3介导的骨重建活性。维生素D3通常协调OB和OC的激活。不平衡的激活OC导致骨吸收。RANK/RANKL/OPG轴被认为是骨质疏松分子机制的关键因素。Mg通过影响甲状旁腺激素和维生素D水平的调节从而影响RANK/RANKL/OPG轴参与骨质疏松的发病机制。影响骨轴和增强OC功能的不同因素导致骨丢失和骨组织微结构损伤,导致骨质疏松症的发生。临床研究表明，补镁可在一定程度上缓解骨质疏松的症状。
