Abstract:

Endometrial polyps (EP) are benign lesions formed by the excessive proliferation of local glands and stroma in the endometrium. They often present as abnormal uterine bleeding and infertility, and the pathogenesis has not been fully elucidated. Current research shows that the pathogenesis of EP is relatively complex, and the relevant mechanisms mainly involve: hormonal and metabolic imbalances, manifested as local estrogen dominance and insulin resistance synergistically promoting endometrial proliferation and inhibiting apoptosis; abnormal cell proliferation and apoptosis, leading to cells escaping programmed death; changes in the inflammatory microenvironment, with abnormal activation of the nuclear factor-κB (NF-κB) pathway and dysfunction of its downstream effector molecules, and co-existence with chronic endometritis; genetic abnormalities, where RAS gene mutations drive polyp growth, and activation of the Wnt signaling pathway further drives polyp clonal proliferation and vascular abnormalities; dysregulation of the genital tract microbiota, where ascending infection by pathogens leads to abnormal repair and hyperplasia of the endometrium and participates in the pathogenesis of EP. This indicates that EP is the result of multifactor and multi-signaling pathway regulation.

Key words: Polyps, Endometrial neoplasms, Endometritis, Hormones, Inflammation, Heredity, Microbiota