骨质疏松症发病率高，发病机理不清，目前尚无有效的治疗措施。老龄化、遗传及激素紊乱等因素会导致骨髓间充质干细胞（BMSC）分化失衡，即倾向分化为脂肪细胞，成骨分化减少。前列腺素在代谢性疾病中有重要作用，目前研究很少机制也不清。我们前期研究发现PGF2α/FP能抑制BMSC的成脂分化而促进成骨分化，在BMSC的表达随年龄增加而降低；蛋白质谱分析发现缺失FP后BMSC成脂分化中H3K27me3的水平增加。我们推测PGF2α/FP通过调节H3K27me3的水平影响BMSC的分化，进而影响骨质疏松症的发展。我们将构建BMSC特异性FP敲除和过表达小鼠，进一步研究PGF2α/FP对骨质疏松症的作用；通过分子生物学手段揭示H3K27me3对FP作用的介导机制；检测针对FP及其下游分子的小分子药物对骨质疏松症的治疗作用。该研究旨在揭示FP在骨质疏松症中的作用及机制，为临床治疗骨质疏松症提供潜在药物靶点。

As a worldwide metabolic disease, the incidence of osteoporosis is high, and the pathogenesis is unclear. At present, there is no effective treatment. Aging, genetic and hormonal disorders and other factors will lead to the imbalance of bone marrow mesenchymal stem cells (BMSC) differentiation, that is, they tend to differentiate into adipocytes. Prostaglandins have an important role in metabolic diseases, and few studies have been conducted to understand the mechanism. Our previous study found that PGF2α/FP inhibited the adipogenic differentiation of BMSC and promote osteogenic differentiation, and the expression in BMSC decreases with age, and protein profile analysis found that the level of H3K27me3 increased in BMSC during adipogenic differentiation when FP was absent. We speculate that PGF2α/FP affects the differentiation of BMSC by regulating the level of H3K27me3, which in turn affects the development of osteoporosis. We will construct BMSC-specific FP knockout and overexpression mice to further study the effect of PGF2α/FP on osteoporosis. Then, we will reveal the mediated mechanism of H3K27me3 on FP through molecular biology. The last but not least, we will detect therapeutic effect of small molecule drugs target FP and its downstream molecules on osteoporosis. This study aims to reveal the role and mechanism of FP in osteoporosis and provide potential drug targets for clinical treatment of osteoporosis.