在衰老机体中,过量的活性氧自由基(ROS)可产生氧化应激(OS),降低骨量和骨质量,诱发骨质疏松.β-catenin与Wnt通路下游的TCF作用可调控骨形成,与FoxO作用可产生抗OS作用,"以衰老和氧化应激为中心"已成为骨质疏松研究的新焦点,抗氧化剂具有防治骨质疏松潜力.%Excessive accumulation of reactive oxygen species ( ROS ) contributes to oxidative stress ( OS ), which results in the decrease of bone mass and bone quality and then in the development of osteoporosis. The interaction between β-catenin and TCF can regulate bone formation mediated by Wnt signaling, but β-catenin can increase defense against OS by binding to FoxO. The "aging and OS-centric" account is a new paradigm of the pathogenesis of osteoporosis, and understanding these mechanisms seem likely to be beneficial to developing antioxidants as a potential therapeutic strategy in the prevention and treatment of osteoporosis.
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