FoxO／Wnt通路在氧化应激介导的骨质疏松中的调控机制

Regulation mechanisum of FoxO/Wnt pathway in osteoporosis mediated by oxidative stress

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 de- velopment 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 thepathogenesis of osteoporosis, and understanding these mecha- nisms seem likely to be beneficial to developing antioxidants as a potential therapeutic strategy in the prevention and treatment of osteoporosis.