ArticleJournal of translational medicine2025
UBE2S-mediated deubiquitination of GLUT1 via USP10 regulates glucose metabolic reprogramming and immune microenvironment to promote fibrosis in endometriosis.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Review
- Microglia-vascular interactions after spinal cord injury: regulatory mechanisms and therapeutic advances.Frontiers in immunology · 2026Review
- From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.Frontiers in immunology · 2026Review
- Ubiquitin-conjugating Enzymes in Cancer.International journal of biological sciences · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundEndometriosis (EM) is a chronic inflammatory disorder characterized by the growth of ectopic endometrial-like tissue and fibrosis. Metabolic reprogramming, particularly enhanced glycolysis, and immune microenvironment dysregulation are key features of EM progression. However, the underlying molecular mechanisms remain poorly understood.
methodsThis study integrated transcriptomic analysis, immunoprecipitation-mass spectrometry (IP-MS), co-immunoprecipitation, and ubiquitination assays to systematically investigate the role of Ubiquitin-Conjugating Enzyme E2S (UBE2S) in regulating glucose metabolism and immune modulation in EM. In vitro, cell experiments, and mouse models were used to validate its effects on glycolysis, macrophage polarization, and fibrosis.
resultsUBE2S was significantly upregulated in ectopic endometrial stromal cells. IP-MS analysis identified glucose transporter 1 (GLUT1) and Ubiquitin-Specific Peptidase 10 (USP10) as key interacting proteins of UBE2S. Mechanistic studies revealed that UBE2S mediates K48-linked deubiquitination of GLUT1 through USP10, stabilizing GLUT1 protein and enhancing glycolytic activity. This metabolic reprogramming leads to lactate accumulation, which induces M2 macrophage polarization and secretion of transforming growth factor β1 (TGF-β1), thereby promoting fibroblast-to-myofibroblast transition and accelerating fibrosis in the lesions. The UBE2S inhibitor cephalomannine significantly downregulated GLUT1 expression, inhibited glycolysis, blocked M2 polarization, and alleviated fibrosis in ectopic lesions.
conclusionThis study reveals the molecular mechanism by which the UBE2S-USP10-GLUT1 axis regulates the immune microenvironment and promotes fibrosis in EM through metabolic reprogramming. Our findings provide new insights into the pathogenesis of EM and offer a theoretical basis for targeting UBE2S in therapeutic strategies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.