ArticleInternational journal of biological sciences2026
SLC25A1-Mediated Cholesterol Accumulation Promotes Endometriosis Progression by Enhancing Endometrial Stromal Cell Proliferation, Invasion, and M2 Macrophage Polarization.
Article in International journal of biological sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Cholesterol metabolic rewiring shapes immune remodeling across hepatocarcinogenesis.Frontiers in immunology · 2026Review
- Associations between aggregate index of systemic inflammation and endometriosis risk utilizing logistic regression analysis.Frontiers in medicine · 2026Article
- RORα: a critical nexus in the crosstalk between cholesterol metabolism and macrophage polarization.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
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 ectopic endometrial stromal cells (EESCs). Furthermore, we identified solute carrier family 25 member 1 (SLC25A1) as a pivotal target for regulating cholesterol metabolism in endometriosis, as it significantly upregulated in ectopic lesions and markedly increased intracellular and extracellular cholesterol content.
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Registered trials
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