Wei Lun, Bo Le, Jiang Wangtao, Qi Ruofan, Luo Chao, Qian Fei, Ma Panjie, Qiu Jianping, Mao Caiping
Reproductive Medicine Center, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Department of Obstetrics and Gynaecology, The Affiliated Suzhou Municipal Hospital of Nanjing Medical University, Suzhou, Jiangsu, China.
Cell Death Discov. 2025 May 27;11(1):255. doi: 10.1038/s41420-025-02531-8.
There is a local renin-angiotensin system (RAS) in the ovary, which is involved in regulating many important physiological processes, but the specific mechanism remains unclear. Polycystic ovarian syndrome (PCOS) is the most frequently reported non-iatrogenic condition with abnormal RAS expression, characterized by overweight or obesity and insulin resistance (IR), both of which are significantly correlated with many long-term complications. These conditions are closely linked to circulatory or local RAS, serving as potential common regulatory nodes. The present study analyzed single-cell RNA sequencing (scRNA-seq) data from mouse ovaries during the reproductive period to obtain the expression levels and location information of RAS components in all cell clusters. It further analyzed the cyclical fluctuations of RAS and the differential gene sets during the estrous cycle. Protein-protein interaction analysis predicted the most closely interacting pathway with RAS, and preliminary evidence of crosstalk between angiotensin II (AngII) and the insulin signaling pathway was identified in the scRNA-seq data. A PCOS mouse model was constructed, replicating clinical reproductive and metabolic complications, and the crosstalk between AngII and IRS1/PI3K/AKT was verified. In conclusion, this study revealed the dynamic changes of the ovarian local RAS at the cellular level during the estrous cycle, and described the role of RAS in regulating ovarian function from a single-cell perspective. It also provided evidence that IR, caused by the crosstalk between AngII and IRS1/PI3K/AKT pathways, may be a potential underlying mechanism of PCOS.
卵巢中存在局部肾素-血管紧张素系统(RAS),该系统参与调节许多重要的生理过程,但其具体机制仍不清楚。多囊卵巢综合征(PCOS)是最常报道的具有RAS表达异常的非医源性病症,其特征为超重或肥胖以及胰岛素抵抗(IR),这两者均与许多长期并发症显著相关。这些病症与循环或局部RAS密切相关,是潜在的共同调节节点。本研究分析了生殖期小鼠卵巢的单细胞RNA测序(scRNA-seq)数据,以获得所有细胞簇中RAS组分的表达水平和定位信息。它进一步分析了发情周期中RAS的周期性波动和差异基因集。蛋白质-蛋白质相互作用分析预测了与RAS相互作用最密切的途径,并且在scRNA-seq数据中鉴定了血管紧张素II(AngII)与胰岛素信号通路之间相互作用的初步证据。构建了PCOS小鼠模型,复制了临床生殖和代谢并发症,并验证了AngII与IRS1/PI3K/AKT之间的相互作用。总之,本研究揭示了发情周期中卵巢局部RAS在细胞水平的动态变化,并从单细胞角度描述了RAS在调节卵巢功能中的作用。它还提供了证据表明,由AngII与IRS1/PI3K/AKT途径之间的相互作用引起的IR可能是PCOS的潜在潜在机制。