Cellular Senescence in Endometrium: A Pivotal Regulator in Physiological Remodeling and Pathological Disorders

TL;DR

Cellular senescence in the endometrium helps with normal tissue renewal but can cause diseases when out of balance.

Contribution

This paper summarizes the role of cellular senescence in endometrial health and disease, highlighting new therapeutic strategies.

Findings

Senescent cells aid in endometrial repair and embryo implantation under normal conditions.

Excess senescent cells contribute to chronic inflammation and reproductive disorders.

Senolytics and SASP inhibitors are potential treatments for endometrial pathologies.

Abstract

As a highly dynamic tissue, the endometrium undergoes complex remodeling during the menstrual cycle and pregnancy. Recent studies have revealed that cellular senescence plays a pivotal role in both physiological renewal (e.g., menstrual shedding, decidualization) and pathological disorders (e.g., endometriosis, intrauterine adhesions, thin endometrium) of the endometrium. Under physiological conditions, senescent cells contribute to tissue repair and embryo implantation through precise regulation. However, pathological accumulation of senescent cells drives chronic inflammation, fibrosis, and reproductive dysfunction. Here we aim to summarize the mechanism indicating endometrial senescence and elucidating their pleiotropic roles in both physiological homeostasis and pathological progression, while discussing emerging therapeutic strategies for clinical translation—including senolytics and SASP inhibitors.

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