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| 基于AGEs/RAGE/NF-κB通路探讨老年性骨质疏松症发病机制 |
| Explore the possible pathogenesis of senile osteoporosis based on AGEs/RAGE/NF-κB pathway |
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| DOI：10.3969/j.issn.1006-7108.2020.06.027 |
| 中文关键词: 糖基化终末产物 糖基化终末产物受体 核因子kappa B 老年性骨质疏松症 |
| 英文关键词:AGEs RAGE NF-κB senile osteoporosis |
| 基金项目:江苏省研究生科学创新计划(SJKY19_1442) |
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| 中文摘要: |
| 随着人口老龄化程度的不断加剧，骨质疏松症发病率已跃居世界慢性病的第三位，骨质疏松及其伴随的疼痛与骨折高风险已成为我国面临的重要公共卫生问题，其中老年性骨质疏症的发病率随着年龄增长呈现显著上升趋势。现阶段，老年性骨质疏症（senile osteoporosis，SOP）的机制研究主要从常规骨代谢信号通路、机械应力、细胞因子以及非编码RNA等方面考虑。最新研究发现，体内糖基化终末产物的堆积能激活核因子kappa B信号通路并诱发氧化应激炎性反应，被认为是导致衰老相关的组织退化的一种潜在机制。 |
| 英文摘要: |
| With the increasing aging of the population, the incidence of osteoporosis has leapt to the third place in the world's chronic diseases. Osteoporosis and its associated pain and high risk of fracture have become an important public health problems in China, including senile.The incidence of osteoporosis showes a significant upward trend with age. At this stage, the mechanism of SOP is mainly considered from the aspects of conventional bone metabolic signaling pathways, mechanical stress, cytokines, and non-coding RNA. Recent studies have found that accumulation of glycosylation end products in vivo activates the nuclear factor kappa B signaling pathway and induces oxidative stress inflammatory responses, which is thought to be a potential mechanism leading to aging-related tissue degradation. |
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