Molecular mechanisms and Biological Functions of Autophagy in Endometrial Diseases

TL;DR

This paper reviews how autophagy, a cellular process, influences endometrial diseases like endometriosis and cancer, and explores its potential as a therapeutic target.

Contribution

The paper provides a comprehensive review of autophagy's molecular mechanisms and dual roles in endometrial health and disease.

Findings

Dysregulated autophagy contributes to endometrial diseases through altered hormone signaling and inflammation.

Autophagy has dual roles in both maintaining endometrial physiology and contributing to pathology.

Targeting autophagy pathways shows therapeutic potential for endometrial diseases.

Abstract

Autophagy is a highly conserved cellular process crucial for maintaining cellular homeostasis by degrading damaged organelles and misfolded proteins. Emerging evidence highlights its pivotal role in endometrial diseases, including endometriosis, endometritis, and endometrial cancer, where dysregulated autophagy contributes to pathogenesis through mechanisms such as altered hormone signaling, inflammation, and metabolic reprogramming. In this review, we comprehensively summarize the molecular machinery of autophagy, its regulatory networks, and its dual roles in endometrial physiology and pathology. Furthermore, we discuss the molecular mechanisms underlying autophagy in endometrial diseases, and the therapeutic potential of targeting autophagy pathways. By integrating recent advances, this review provides insights into autophagy's complex interplay with endometrial diseases and its implications for future research and therapeutic applications.

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