A genetically engineered mouse model for ovarian hyperstimulation syndrome.

Abstract

Ovarian hyperstimulation syndrome (OHSS) is a common iatrogenic complication resulting from ovarian stimulation in assisted reproductive technology (ART). Excessive stimulation by follicle-stimulating hormone (FSH) has been recognized as a primary cause of OHSS. However, understanding the pathophysiological mechanisms of OHSS and developing effective drugs have been limited due to the absence of suitable animal models. In this study, we generated a FSH gene knock-in (FKI) mouse model to inducible FSH expression by the Tet-on system, that reflects the clinical manifestations of OHSS in patients. Upon administration of doxycycline (Dox), the FKI mice exhibited significantly elevated serum FSH levels compared to their wild-type (WT) littermate controls, accompanied by increased levels of estradiol (E2) and luteinizing hormone (LH), ovarian enlargement, and enhanced peritoneal permeability. Thus, the FKI mouse model is a valuable tool for studying OHSS, particularly dissecting the pathophysiological mechanism and developing potential prevention strategies.