Abstract

The human endometrium plays a vital role in providing the site for embryo implantation and maintaining the normal development and survival of the embryo. Recent studies have shown that stress is a common factor for the development of unexplained reproductive disorders. The nonreceptive endometrium and disturbed early maternal-fetal interaction might lead to infertility including the repeated embryo implantation failure and recurrent spontaneous abortion, or late pregnancy complications, thereby affecting the quality of life as well as the psychological status of the affected individuals. Additionally, psychological stress might also adversely affect female reproductive health. In recent years, several basic and clinical studies have tried to investigate the harm caused by psychological stress to reproductive health, however, the mechanism is still unclear. Here, we review the relationship between psychological stress and endometrial dysfunction, and its consequent effects on female infertility to provide new insights for clinical therapeutic interventions in the future.

Highlights

  • Infertility is a disease characterized by the failure to establish a clinical pregnancy after 12 months of regular and unprotected intercourse

  • Psychological stress includes the physiological reaction to threat or pressure, which is common in various physical illnesses and is increasingly recognized as a risk factor for disease onset and progression

  • Many studies have indicated that psychological stress might be an important risk factor underlying infertility

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Summary

Introduction

Infertility is a disease characterized by the failure to establish a clinical pregnancy after 12 months of regular and unprotected intercourse. The embryo implantation occurs in the functional layer of the endometrium, which is regulated by changes in the ovarian hormones, mainly progesterone and estrogen. The local levels of autocrine and paracrine molecules change during the menstrual cycle and play an important role for directing the establishment of uterine receptivity [41, 42].

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Conclusion

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