ReviewPharmaceuticals (Basel, Switzerland)2025
Warburg-like Metabolic Reprogramming in Endometriosis: From Molecular Mechanisms to Therapeutic Approaches.
Review in Pharmaceuticals (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Changes in the metabolism of axillary lymph node cells as a predictor of regional metastasis in breast cancer.World journal of experimental medicine · 2026Article
- Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.iScience · 2026Review
- The endometriosis-adenomyosis spectrum: shared pathophysiology and microenvironment-driven disease divergence.Reproductive biology and endocrinology : RB&E · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Glycolytic reprogramming in endometriosis: molecular mechanisms, immune modulation, and non-hormonal therapeutic opportunities.BMC women's health · 2026Review
- O-GlcNAc modification regulates autophagy and apoptosis in endometriosis.Functional & integrative genomics · 2026Article
- Is Recurrent Endometriosis a Reprogrammed Disease? Molecular Persistence Beyond Surgical Clearance.Cells · 2026Review
- Cancer-like Hallmarks of Endometriosis: The Role of Estrogen Signaling and Stem Cell Plasticity.International journal of molecular sciences · 2026Review
- Stromal cell-derived itaconate promotes endometriosis via macrophage NRF2 and lysosomal pH modulation.Redox biology · 2026Article
- Pathogenesis of Adenomyosis: An Integrated Review of Cellular Origins, Molecular Mechanisms, and Intersecting Diseases.Journal of cellular and molecular medicine · 2026Review
- Integrating Metabolic and MicroRNA Profiling to the Diagnostics of Endometriosis: A Pilot Study.International journal of molecular sciences · 2026Article
- Review
- Immune-epigenetic-metabolic crosstalk: attempting to unravel the multidimensional mechanisms of immune evasion in endometriosis.Frontiers in immunology · 2026Review
- Multi-omics Mendelian randomization identifies mitochondrial genes associated with immune microenvironment signatures in endometriosis.Frontiers in reproductive health · 2026Article
- Mitochondria in health and disease: cellular powerhouses, signaling centers, and drivers of dysfunction.Frontiers in cell and developmental biology · 2026Review
- Closing the evidence loop-membrane-lipid homeostasis and vesicular transport link DEHP exposure to endometriosis.Human genomics · 2025Article
- Dynamics of Conventional Metabolic Indices in Relation to Endometriosis Severity: A Retrospective Analysis.International journal of general medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Endometriosis is a chronic gynecological disorder characterized by the presence of endometrial-like tissue outside the uterus, leading to inflammation, pain, and infertility. Emerging evidence indicates that endometriotic lesions exhibit cancer-like properties, including metabolic reprogramming marked by increased glucose uptake, enhanced Warburg's effect, and altered mitochondrial function. These metabolic adaptations support cell survival under hypoxic conditions and contribute to immune evasion and sustained proliferation. This review summarizes current findings on the molecular mechanisms driving metabolic reprogramming in endometriosis, including the roles of mitochondrial dysfunction, hypoxia-inducible factor (HIF) signaling, the PI3K/AKT/mTOR pathway, inflammatory cytokines, and genetic and epigenetic regulators. In addition, we discuss therapeutic strategies targeting glycolytic pathways using both synthetic inhibitors and natural compounds, which represent promising non-hormonal options. Finally, we highlight the need for further preclinical and clinical studies to validate metabolic interventions and improve outcomes for patients with endometriosis.
Indexed as
Identifiers
What Socratic holds
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.