Accumulating evidence indicates that intracellular reactive oxygen species (ROS) production is highly involved in bone homeostasis by intervening osteoclast or osteoblast differentiation. Interestingly, ROS that are known as oxidizing agents exert dose-dependent biphasic properties in bone remodeling, including preventing osteoblast activity but accelerating osteoclast resorption. ROS mainly composed of superoxide anion radical, hydroxyl radical, nitric oxide, and two-electron reduction product hydrogen peroxide, which are important components to regulate bone cell metabolism and function in mammal skeleton. These free radicals can be partly produced in bone and boosted in an inflammation state. Although numerous researches have emphasized the impacts of ROS on bone cell biology and verified the mechanism of ROS signaling cascades, the recapitulatory commentary is necessary. In this review article, we particularly focus on the regulation of the intracellular ROS and its potential mechanism impacting on cell-signaling transduction in osteoclast and osteoblast differentiation for preferable understanding the pathogenesis and searching for novel therapeutic protocols for human bone diseases.

中文翻译：

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ROS信号级联反应：破骨细胞和成骨细胞的双重调控

越来越多的证据表明，通过干预破骨细胞或成骨细胞的分化，细胞内活性氧（ROS）的产生与骨稳态高度相关。有趣的是，被称为氧化剂的ROS在骨骼重塑中发挥剂量依赖性的双相特性，包括阻止成骨细胞活性但加速破骨细胞吸收。ROS主要由超氧阴离子自由基，羟基自由基，一氧化氮和二电子还原产物过氧化氢组成，它们是调节骨骼细胞代谢和在哺乳动物骨骼中起作用的重要成分。这些自由基可在骨骼中部分产生，并在炎症状态下增强。尽管许多研究都强调了ROS对骨细胞生物学的影响并验证了ROS信号级联的机制，总结性评论是必要的。在这篇综述文章中，我们特别关注细胞内ROS的调节及其对破骨细胞和成骨细胞分化中细胞信号转导的影响的潜在机制，以更好地了解人类骨骼疾病的发病机理并寻找新的治疗方案。