硒代半胱氨酸
硒蛋白
硫氧还蛋白还原酶
硒蛋白P
谷胱甘肽过氧化物酶
硫氧还蛋白
GPX4
GPX1型
化学
抗氧化剂
内分泌学
内科学
氧化应激
细胞生物学
生物
生物化学
医学
酶
超氧化物歧化酶
半胱氨酸
作者
Zhichao Zhang,Jinsong Zhang,Jianru Xiao
标识
DOI:10.1016/j.bbagen.2014.08.001
摘要
Emerging evidence supports the view that selenoproteins are essential for maintaining bone health. The current state of knowledge concerning selenoproteins and Se status in bone physiology and pathology is summarized. Antioxidant selenoproteins including glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), as a whole, play a pivotal role in maintaining bone homeostasis and protecting against bone loss. GPx1, a major antioxidant enzyme in osteoclasts, is up-regulated by estrogen, an endogenous inhibitor of osteoclastogenesis. TrxR1 is an immediate early gene in response to 1α,25-dihydroxyvitamin D3, an osteoblastic differentiation agent. The combination of 1α,25-dihydroxyvitamin D3 and Se generates a synergistic elevation of TrxR activity in Se-deficient osteoblasts. Of particular concern, pleiotropic TrxR1 is implicated in promoting NFκB activation. Coincidentally, TrxR inhibitors such as curcumin and gold compounds exhibit potent osteoclastogenesis inhibitory activity. Studies in patients with the mutations of selenocysteine insertion sequence-binding protein 2, a key trans-acting factor for the co-translational insertion of selenocysteine into selenoproteins have clearly established a causal link of selenoproteins in bone development. Se transport to bone relies on selenoprotein P. Plasma selenoprotein P concentrations have been found to be positively correlated with bone mineral density in elderly women. A full understanding of the role and function of selenoproteins and Se status on bone physiology and pathology may lead to effectively prevent against or modify bone diseases by using Se.
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