Molecular Mechanisms of Endometrial Functioning in Women with Polycystic Ovary Syndrome

Endocrinologic and metabolic abnormalities in polycystic ovary syndrome (PCOS) may have complex effects on the endometrium, contributing to the infertility endometrial disorders observed women with this  syndrome. The consequences of PCOS on homeostasis pathophysiology not been comprehensively understood. This review provides an overview molecular mechanisms endometrial  function with this pathology. Analysis literature data found that changes estrogen and progesterone violation spatial temporal expression steroid receptors. In PCOS impaired follicle maturation consequent anovulation cause a chronic progesterone-deficient state affects the milieu. Furthermore, even ovulation (and thus acting endometrium), PCOS endometrium has several including altered pattern receptivity markers during the period implantation glucose transporter 4 (GLUT4) as well progesterone-resistance. These pathological phenomena explain possible increasing cell proliferation. An imbal ance adipose tissue worsens increase estrogen levels its pathological effects. Hyperandrogenia and hyperinsulinemia lead disruption cellular proliferation apoptosis, affect insulin signaling glucose metabolism, disrupting energy homeostasis. Inflammation oxidative stress endometrium are closely related, increased endometrium. can induce production inflammatory cytokines this directly stimulates excess  ovarian androgen production. The potential underlying these disorders, specifically PCOS, are await additional transdisciplinary research for their complete elucidation.