SLC25A1-Mediated Cholesterol Accumulation Promotes Endometriosis Progression by Enhancing Endometrial Stromal Cell Proliferation, Invasion, and M2 Macrophage Polarization.

ABSTRACT: Endometriosis is an estrogen-dependent chronic inflammatory disorder. Cholesterol (CHO) has been reported to be closely associated with estrogen synthesis and inflammatory responses. Nevertheless, the mechanisms underlying the effects of cholesterol on endometriosis progression and immune response remain to be elucidated. Our research revealed that cholesterol accumulation in ectopic lesions acts as a crucial catalyst for the progression of endometriosis. Using a co-culture system, we simulated a cholesterol-abundant ectopic milieu and demonstrated cholesterol induced M2 macrophage polarization via the STAT6/PPARγ pathway, connecting cholesterol metabolism to immune response in endometriosis. Notably, cholesterol-induced M2 macrophage polarization accelerated the aggressive behavior of ect

SUBMITTER: Yang P 

PROVIDER: S-EPMC12681928 | biostudies-literature | 2026

REPOSITORIES: biostudies-literature