Endometrial receptivity and embryo implantation are the key steps to determine the success of pregnancy. Stress factor is an important risk factor for early pregnancy failure, and its pathological mechanism is unknown. The applicant's previous studies have found that adrenergic signals are involved in regulating the physiological and pathological processes of early pregnancy. Monoamine oxidase (MAO) is an important regulator of stress and participates in the metabolism of epinephrine and other monoamines. Studies have shown that MAO is specifically over expressed in the endometrium during the receptive phase. This research focuses on the early pregnancy process. We further explore the role of MAO-mediated monoamine homeostasis in regulating the function of the uterus during the periimplantation period by using MAO-specific inhibitors, stress mice models and transgenic mice models. On this basis, the molecular mechanism of MAO-mediated monoamine homeostasis affecting the function of endometrium during periimplantation was further studied by using organoid and stromal cell-induced decidualization models, combined with transcriptome sequencing and other technical methods. Our study provide theoretical basis for the formulation of timely and effective clinical intervention strategies, and alleviate the heavy reproductive burden and social problems caused by anxiety.
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