ArticleThe Journal of clinical investigation2024
TET3-overexpressing macrophages promote endometriosis.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The trial behind it
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Who cites it
18 citing papers in PubMed.
- Trophoblast Extracellular Vesicles Rewire Immunity: A Symptom-Relief Avenue for Recessive Dystrophic Epidermolysis Bullosa.Journal of extracellular vesicles · 2026Article
- Single-Cell RNA Sequencing Shows Markedly Elevated Immune Cell Proportions in the Endometrium of Women with Endometriosis-A Narrative Review.International journal of molecular sciences · 2026Review
- The Role of Macrophages in Endometrial Cyclical Changes and Female Reproductive System Diseases: A Review.Current issues in molecular biology · 2026Review
- Pyruvate carboxylase promotes SREBP1a-mediated lipid synthesis in epithelial ovarian cancer.Communications biology · 2026Article
- Redefining the contribution of retrograde menstruation to endometriosis: single-cell analysis of endometriotic lesions suggests a process more complex than simple autografting.Molecular medicine (Cambridge, Mass.) · 2026Article
- Metabolic-epigenetic imprinting of macrophages in endometriosis: a working model for lesion persistence and treatment.Frontiers in immunology · 2026Review
- Immune-epigenetic-metabolic crosstalk: attempting to unravel the multidimensional mechanisms of immune evasion in endometriosis.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
- Identifying serum microRNAs as biomarkers for endometriosis in adolescents and young adults.Reproductive biology and endocrinology : RB&E · 2025Article
- TET3-overexpressing macrophages are a unifying pathogenic feature with therapeutic potential in chronic inflammatory diseases.The Journal of clinical investigation · 2025Review
- TET3 is a regulator and can be targeted for the intervention of myocardial fibrosis.EMBO molecular medicine · 2025Article
- MYC/TET3-Regulated TMEM65 Activates OXPHOS-SERPINB3 Pathway to Promote Progression and Cisplatin Resistance in Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Precision Therapeutic and Preventive Molecular Strategies for Endometriosis-Associated Infertility.International journal of molecular sciences · 2025Review
- Exploring the Immune System's Role in Endometriosis: Insights Into Pathogenesis, Pain, and Treatment.Cureus · 2025Review
- Crosstalk between metabolism and epigenetics during macrophage polarization.Epigenetics & chromatin · 2025Review
- Epitranscriptomic Modulation of TET2 Inhibition Suppressed SARS-CoV-2 Infection and Blocked Viral Nucleocapsid Protein in Induced-Pluripotent-Stem-Cell-Derived Cardiomyocyte Screening Models.Biomaterials research · 2025Article
- Update on the pathogenesis of endometriosis-related infertility based on contemporary evidence.Frontiers in endocrinology · 2025Review
- Targeting TET3 in macrophages provides a concept strategy for the treatment of endometriosis.The Journal of clinical investigation · 2024Article
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
Endometriosis is a debilitating, chronic inflammatory disease affecting approximately 10% of reproductive-age women worldwide with no cure. While macrophages have been intrinsically linked to the pathophysiology of endometriosis, targeting them therapeutically has been extremely challenging due to their high heterogeneity and because these disease-associated macrophages (DAMs) can be either pathogenic or protective. Here, we report identification of pathogenic macrophages characterized by TET3 overexpression in human endometriosis lesions. We show that factors from the disease microenvironment upregulated TET3 expression, transforming macrophages into pathogenic DAMs. TET3 overexpression stimulated proinflammatory cytokine production via a feedback mechanism involving inhibition of let-7 miRNA expression. Remarkably, these cells relied on TET3 overexpression for survival and hence were vulnerable to TET3 knockdown. We demonstrated that Bobcat339, a synthetic cytosine derivative, triggered TET3 degradation in both human and mouse macrophages. This degradation was dependent on a von Hippel-Lindau (VHL) E3 ubiquitin ligase whose expression was also upregulated in TET3-overexpressing macrophages. Furthermore, depleting TET3-overexpressing macrophages either through myeloid-specific Tet3 ablation or using Bobcat339 strongly inhibited endometriosis progression in mice. Our results defined TET3-overexpressing macrophages as key pathogenic contributors to and attractive therapeutic targets for endometriosis. Our findings may also be applicable to other chronic inflammatory diseases where DAMs have important roles.
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