Endometriosis Research and Treatment

Interleukin-4 suppresses TIMP-2 transcription during endometriosis: Allele-specific regulation of the TIMP-2 -418G/C promoter by SP1

This study identifies an IL-4-SP1-TIMP-2 regulatory axis that contributes to ECM dysregulation in endometriosis and shows the TIMP-2 -418G/C promoter polymorphism affects cytokine-mediated transcription.

High-Resolution Spatial Transcriptomics Reveals Fibroblast and Neuroimmune Microenvironments in Endometriosis Lesions

This study uses high-resolution spatial transcriptomics to map fibroblast and neuroimmune microenvironments in endometriosis lesions, identifying spatial cellular interactions linked to pain.

Hormonal factors are poor indicators of endometriosis pain

This study examines the relationship between sex hormone levels and endometriosis-related pain in women, finding weak associations between specific receptor transcript levels and pain intensity.

Simvastatin and Primaquine Identified as Potential Endometriosis Therapeutics via a Novel Epithelial-Stromal Assembloid Drug Screening Assay

The paper identifies simvastatin and primaquine as potential endometriosis treatments using human assembloids, showing significant reversal of disease-related gene expression pathways.

Predicting Endometriosis Status and Menstrual Cycle Phase Using DNA Methylation

This study uses DNA methylation data to predict endometriosis status and menstrual cycle phase, finding strong performance for cycle phase and moderate performance for endometriosis.

Preferential innervation of endometriosis by hyperexcitable Ret/GFRα1+ nociceptors associates with target GDNF and clinical pain

The paper identifies hyperexcitable Ret/GFRα1+ nociceptors innervating endometriosis lesions that correlate with GDNF levels and clinical pain.

A Transcriptomics-Based Computational Drug Repurposing Pipeline Identifies Simvastatin And Primaquine As Therapeutics For Endometriosis

This study identifies simvastatin and primaquine as potential therapeutics for endometriosis through computational drug repositioning, showing reduced pain and gene expression changes in animal models and lower disease risk in EMR data.

Site-dependent transcriptomic signatures of endometriosis are conserved across hormonal states

The paper identifies core lesion cells in endometriosis that retain uterine transcriptomic identity across hormonal states and uses them to classify disease status and lesion subtype.

Metabolomic signatures support the diagnostics of peritoneal endometriosis using generalised linear models.

This study identifies metabolite ratios using generalized linear models to diagnose peritoneal endometriosis with high accuracy from plasma samples.

The over-activated peritoneal immune environment in endometriosis is characterised by a lack of PD-1 inhibition.

This study identifies reduced PD-1 expression in peritoneal fluid of endometriosis patients, suggesting its role in persistent inflammation and potential as a therapeutic target.

Decoding the regulatory genetic architecture of endometriosis using AlphaGenome

This paper uses AlphaGenome to prioritize endometriosis-associated variants with strong uterus-specific regulatory effects, identifying new candidate genes and refining GWAS loci.

Genetic liability for endometriosis associates with pain, inflammatory, and metabolic traits: a polygenic score analysis

This paper uses a polygenic risk score to show that genetic liability for endometriosis is linked to pain, inflammatory, and metabolic traits in both sexes.

An investigation of the IL-23/Th17 axis and transcriptomic profiles of T helper subsets in endometriosis

This study investigates the IL-23/Th17 axis and transcriptomic profiles of T helper subsets in endometriosis, revealing immune remodeling and a distinct Th17 cell phenotype.

RE-1 silencing transcription factor is reduced in endometriosis and uterine deletion in mice alters progesterone responsiveness

This study shows REST is reduced in endometriosis and its deletion in mice causes progesterone resistance, subfertility, and larger endometriotic lesions.

Whole-genome methylation profiling of menstrual stem cells identifies novel biomarkers for endometriosis

The paper identifies DNA methylation biomarkers in menstrual stem cells that distinguish endometriosis from controls with high diagnostic accuracy.

Contributions of T helper 9 cells in endometriosis-associated inflammation and lesion growth

This study investigates the role of Th9 cells in endometriosis by analyzing human tissue samples, in vitro experiments, and a mouse model, finding increased IL-9-positive cells and pro-inflammatory mediators in lesions.

Transferrin participates in the pathogenesis of endometriosis by influencing the proliferation, migration and apoptosis of endometrial cells

This study shows that transferrin promotes endometriosis by enhancing endometrial stromal cell proliferation, migration, and reducing apoptosis.

Preconceptional immunomodulation partially corrects pregnancy associated abnormalities induced by endometriosis in a mice model, with a normalization of transcriptional alteration observed in the developing fetal maternal interface at the single cell level.

This study shows that preconceptional immunomodulation reduces pregnancy complications in a mouse model of endometriosis by partially reversing transcriptional changes in fetal-maternal interfaces.

Endometriosis lesions are oligoclonal structures derived from the normal endometrium

This study shows endometriosis lesions originate from the normal endometrium through clonal expansion, with distinct clones at different body sites.

RNA foundation models enable generalizable endometriosis disease classification and stable gene-level interpretation

This paper uses RNA foundation models to improve endometriosis classification across cohorts and identifies stable gene-level predictors.

Neurobiological Signatures of Endometriosis: Characterizing Pain, Cognition, and Brain Morphology

This study investigates the neurobiological correlates of endometriosis by integrating neuroimaging, biofluids, and cognitive assessments, finding pain-related brain structure and microstructure changes in affected individuals.

Compound design of a patient-derived 3D cell culture system modelling early peritoneal endometriosis

This paper develops a 3D patient-derived co-culture model of early peritoneal endometriosis to study lesion formation and progression.

Beyond one-size-fits-all: single-cell transcriptomic signatures predict drug efficacy and reveal responder subgroups in endometriosis

This paper uses single-cell transcriptomics to identify drug response subgroups and therapeutic targets in endometriosis, revealing tissue-specific and inter-patient heterogeneity.

Establishment and Characterization of a New Immortalized Human Adenomyosis Epithelial-Like Cell Line, tAEC21

This paper establishes and characterizes a new immortalized human adenomyosis epithelial-like cell line, tAEC21, which exhibits specific marker expression and functional responses relevant to adenomyosis.

Defects in the DNA Damage Response of Patient-derived Endometriosis Stromal Cells

This study shows that endometriosis patient-derived stromal cells have a defective DNA damage response, leading to reduced senescence and altered DDR activation under replication stress.

Hemin Inhibits the Activation of STING in Macrophages by Inducing HO-1, Promoting Endometriosis Development

This study shows hemin induces HO-1 in macrophages, inhibiting STING pathway activation and promoting endometriosis development.

Pro-endometriosis macrophage release of IL-33 is key for endometriosis pain and lesion formation

This study identifies IL-33 as a key mediator in endometriosis pain and lesion formation through neuroimmune communication involving CGRP and macrophages.

Deconvolution of bulk endometrial tissue identifies cell type proportions and expression signatures associated with endometrial function and disease

The paper uses deconvolution on bulk RNA-seq data to identify cell type proportions and expression signatures linked to endometrial function and disease in women with and without endometriosis.

Rethinking the Estrogen Receptor Beta Dominance Hypothesis in Endometriosis: Insights from Single Cell RNA Sequencing Meta-analysis

This study challenges the ER{beta} dominance hypothesis by showing no significant ER{beta} dominance in endometriosis tissues and highlighting cell- and tissue-specific roles of estrogen receptor isoforms.

M2 Macrophages are Major Mediators of Germline Risk of Endometriosis and Explain Pleiotropy with Comorbid Traits

This study identifies M2 macrophages and IL1 signaling as key mediators of endometriosis risk and shows their pleiotropic role in comorbid traits.