卵巢衰老伴随着卵母细胞质量降低，严重危害女性生殖健康。研究表明线粒体数量和质量异常是造成卵母细胞质量降低的关键因素。线粒体Lon蛋白酶（Lonp1）是一种ATP依赖的线粒体丝氨酸蛋白酶，参与线粒体质量调控。我们前期研究证实，老龄小鼠卵母细胞Lonp1表达降低；卵母细胞特异性敲除Lonp1小鼠不孕，各级卵泡数量减少，卵母细胞胞质皱缩，纺锤体形成异常；进一步发现Lonp1敲除小鼠卵母细胞线粒体内蛋白堆积且非折叠蛋白反应（mtUPR）异常激活。推测Lonp1通过介导卵母细胞mtUPR参与卵母细胞质量控制。本项目拟在前期工作基础上，从临床样本、卵母细胞Lonp1敲除动物模型等层面明确Lonp1在高龄患者和小鼠卵母细胞中的动态表达模式以及与卵母细胞质量的关系，进而探究Lonp1在卵母细胞质量控制中的新分子机制，以期阐明部分高龄患者卵母细胞质量低下的病理分子机制。

Ovarian aging is accompanied by a decline in the quality of oocytes, which seriously endangers female reproductive health. Studies have shown that abnormal mitochondrial quantity and quality are key factors that cause oocyte quality to decline. Mitochondrial Lon protease (Lonp1) is an ATP-dependent mitochondrial serine protease that is associated with the regulation of mitochondrial quality. Our previous research confirmed that the expression of Lonp1 in oocytes of aged mice was reduced and oocyte specific knockout Lonp1 leads to infertility. The number of follicles at all stages was decreased in oocyte specific knockout Lonp1 mice, with oocyte cytoplasmic shrinkage and abnormal spindle formation. Further it is found that Lonp1 knockout mouse oocytes have mitochondrial protein accumulation and abnormally unfolded protein response (mtUPR) activation. It is speculated that Lonp1 participates in oocyte quality control by mediating oocyte mtUPR. Based on the preliminary work, this project intends to clarify the dynamic expression pattern of Lonp1 in elderly patients and mouse oocytes from clinical samples and oocyte Lonp1 knockout mice model, to explore the relationship between the content of Lonp1 and oocyte quality. Further we will explore the new molecular mechanism of Lonp1 in the quality control of oocytes, to clarify the new molecular mechanism of the oocytes with low quality in some elderly patients.