ArticleThe Journal of clinical endocrinology and metabolism2014
Transforming growth factor-β induced Warburg-like metabolic reprogramming may underpin the development of peritoneal endometriosis.
Article in The Journal of clinical endocrinology and metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
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Who cites it
89 citing papers in PubMed, 156 citations in OpenAlex.
- YTHDF3 promotes angiogenesis in endometriosis by enhancing the translation efficiency of PFKFB3.Angiogenesis · 2026Article
- Glycolytic Reprogramming in Endometriosis: Biological Basis and Emerging Targets for Disease-Modifying Therapy.Journal of clinical medicine · 2026Review
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- The lactate-myeloid-derived suppressor cells axis in endometriosis from molecular reprogramming to translational therapies: A review article.International journal of reproductive biomedicine · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Endometriosis-related alterations in the endometrium revealed by integrated single-cell and AI-powered approaches.Nature communications · 2026Article
- Lactate and lactylation: mechanisms, function, diseases, and therapeutic targets.Molecular biomedicine · 2026Review
- Association between circulating metabolites and endometriosis: a bidirectional two-sample Mendelian randomization study.Obstetrics & gynecology science · 2026Article
- Immune-epigenetic-metabolic crosstalk: attempting to unravel the multidimensional mechanisms of immune evasion in endometriosis.Frontiers in immunology · 2026Review
- Dysregulation of Key Biological Processes in Endometriosis Pathophysiology.Current molecular medicine · 2026Review
- Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.Frontiers in immunology · 2026Review
- BDNF facilitates ectopic endometrial stromal cell growth, invasion, migration and glycolysis in endometriosis via upregulating GLUT1.CytoJournal · 2026Article
- Metabolic-epigenetic imprinting of macrophages in endometriosis: a working model for lesion persistence and treatment.Frontiers in immunology · 2026Review
- Immune Suppression and Somatic Mutation in Endometriosis - An Opportunity for Personalized Immunotherapy.International journal of women's health · 2026Article
- Endometrial Stromal Cells from Endometriosis Patients Reflect Lesion-Type-Specific Heterogeneity.Cells · 2025Article
- Endometriosis: new insights and opportunities for relief of symptoms.Biology of reproduction · 2025Review
- Identification of metabolic reprogramming-associated biomarkers in endometriosis through integrated bioinformatics analysis.Hereditas · 2025Article
- Dual Targeting of Orphan Nuclear Receptors NR4A1 and NR4A2 for Nonhormonal Endometriosis Therapy.Endocrinology · 2025Article
- Precision Therapeutic and Preventive Molecular Strategies for Endometriosis-Associated Infertility.International journal of molecular sciences · 2025Review
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
contextTGF-β is believed to play a major role in the etiology of peritoneal endometriosis. In tumors, TGF-β induces the metabolic conversion of glucose to lactate via glycolysis, a process referred to as the "Warburg effect." Lactate increases cell invasion, angiogenesis, and immune suppression, all crucial steps in the development of endometriosis.
objectiveThe aim of this study was to determine whether TGF-β induces a "Warburg-like" effect in peritoneal endometriosis.
designThe study was informed by human tissue analysis and cel culture.
settingThe study was conducted at the university research institute. PATIENTS OR OTHER
participantsWe studied women undergoing surgical investigation for endometriosis.
interventionsConcentrations of lactate and TGF-β1 in peritoneal fluid (n = 16) were measured by commercial assay. Expression of genes implicated in glycolysis was measured in endometrial and peritoneal biopsies (n = 31) by quantitative RT-PCR and immunohistochemistry. The effect of TGF-β1 on primary human peritoneal mesothelial cells (n = 6) and immortalized mesothelial (MeT-5A) cells (n = 3) was assessed by quantitative RT-PCR, Western blot, and commercial assays.
main outcome measuresLactate, TGF-β1, and markers of glycolysis were measured.
resultsConcentrations of lactate in peritoneal fluid paralleled those of TGF-β1, being significantly higher in women with endometriosis compared to women without (P < .05). Endometriosis lesions expressed higher levels of glycolysis-associated genes HIF1A, PDK1, and LDHA than eutopic endometrium, and adjacent peritoneum had higher levels of HIF1A and SLC2A1 than peritoneum from women without disease (P < .05 to P < .001). Exposure of mesothelial cells to TGF-β1 increased production of lactate (P < .05), increased HIF1A mRNA (P < .05), and protein, and increased concentrations of mRNAs encoded by glycolysis-associated genes (LDHA, PDK1, SLC2A1; P < .05).
conclusionsA change in the metabolic phenotype of endometriosis lesions and peritoneal mesothelium in women with endometriosis may favor development of endometriosis.
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Registered trials
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