髓系抑制性细胞（MDSCs）是一群骨髓来源的不成熟的，处于不同状态的异质性细胞的总称。随着年龄增长，MDSCs在骨髓腔中大量募集。骨髓微环境中的MDSCs是一种新型破骨前体细胞，具备直接破骨分化及骨吸收的能力。晚期氧化蛋白产物（AOPPs）是一种致病介质，其在体内蓄积水平与年龄呈正相关。AOPPs可通过破坏骨形成-骨吸收偶联，导致骨量丢失及骨组织微结构破坏，进而参与骨质疏松症的发病过程。预实验结果表明：AOPPs可诱导MDSCs髓内募集及破骨分化。本项目通过体内、体外实验深入研究：1）AOPPs诱导MDSCs髓内募集及破骨分化的作用，及其与骨量丢失的相关性；2）AOPPs诱导MDSCs破骨分化的分子机制；3）阻断AOPPs诱导的MDSCs破骨分化对骨量丢失及骨质疏松症的干预作用。从而为老年性骨质疏松症的防治提供新思路。

Myeloid-derived suppressor cells (MDSCs) are a heterogeneous population comprising immature myeloid cells with an immunosuppressive effect. MDSCs expansion in marrow cavity is age related. MDSCs in bone marrow microenvironment were a novel kind of osteoclast progenitor. In certain circumstances, MDSCs could differentiate into functional osteoclasts. Advanced oxidation protein products (AOPPs) are a kind of endogenous pathological mediator. The accumulation of AOPPs in vivo is positively correlated with age. AOPPs accumulation could induce bone loss and bone microstructure deterioration by interfering the dynamic balance between bone formation and bone resorption. Our preliminary experiment results showed that AOPPs could induce MDSCs expansion and osteoclast differentiation. By in vivo and in vitro studies, our project will clarify: 1）The effect of AOPPs induced MDSCs expansion and osteoclast differentiation, and its relationship with bone loss; 2）The molecular mechanism of AOPPs induced MDSCs osteoclast differentiation; 3）Blocking AOPPs induced MDSCs osteoclast differentiation, and examine its effect in age related bone loss and osteoporosis. This study may develop a novel strategy for the prevention and intervention of senile osteoporosis.