The ovary is a female reproductive organ that plays a key role in fertility and the maintenance of endocrine homeostasis, which is of great importance to women’s health. It is characterized by a high heterogeneity, with different cellular subpopulations primarily containing oocytes, granulosa cells, stromal cells, endothelial cells, vascular smooth muscle cells, and diverse immune cell types. Each has unique and important functions. From the fetal period to old age, the ovary experiences continuous structural and functional changes, with the gene expression of each cell type undergoing dramatic changes. In addition, ovarian development strongly relies on the communication between germ and somatic cells. Compared to traditional bulk RNA sequencing techniques, the single-cell RNA sequencing (scRNA-seq) approach has substantial advantages in analyzing individual cells within an ever-changing and complicated tissue, classifying them into cell types, characterizing single cells, delineating the cellular developmental trajectory, and studying cell-to-cell interactions. In this review, we present single-cell transcriptome mapping of the ovary, summarize the characteristics of the important constituent cells of the ovary and the critical cellular developmental processes, and describe key signaling pathways for cell-to-cell communication in the ovary, as revealed by scRNA-seq. This review will undoubtedly improve our understanding of the characteristics of ovarian cells and development, thus enabling the identification of novel therapeutic targets for ovarian-related diseases.

Background: Various controversial conclusions exist regarding the reproductive toxicity of cyclophosphamide, creating uncertainties about the recovery timeline of maternal reproductive capacity and offspring health. Methods: Using a mouse model with a clinically relevant cyclophosphamide dosing regimen, we examined the recovery of female reproductive function after exposure and the long-term survival and development of their offspring. Results: Our findings revealed that cyclophosphamide exposure shortened the maternal reproductive lifespan, characterized by early fertility impairment at one week (p < 0.05), transient recovery at two weeks (p > 0.05), a subsequent decline at four weeks with further deterioration, and eventual progression to infertility at six months (p < 0.01). F1 pups from the cyclophosphamide group exhibited growth restriction, higher mortality rates, delayed pubertal onset, and impaired neurodevelopment during long-term follow-up. Although some parameters transiently improved at 2 weeks post-withdrawal, these abnormalities persisted or recurred at 4 and 8 weeks, indicating that developmental defects were not lessened by prolonging the medication withdrawal period. Conclusions: These findings demonstrate irreversible gonadotoxicity and developmental toxicity following cyclophosphamide exposure in this mouse model.