Studies

Building on a transcriptomics-based computational drug-repositioning pipeline (which previously identified fenoprofen), the researchers evaluated two further candidates, simvastatin (a statin) and primaquine (an antimalarial). In a rat model of endometriosis-associated pain, both drugs reduced pain-associated behaviors and reversed endometriosis-related gene-expression changes (assessed via behavioral testing and bulk RNA sequencing). In addition, a retrospective analysis of electronic medical records across six University of California healthcare institutions found that simvastatin prescription was associated with a lower relative risk of an endometriosis diagnosis. The results support both drugs as candidates for repurposing and the value of computational drug repositioning, though clinical trials are still needed.

This observational steroid-profiling study compared serum androgen patterns in women with laparoscopically confirmed endometriosis and healthy controls. It identified a distinct hormonal signature, including altered adrenal-androgen concentrations and higher 11-ketotestosterone levels, and metabolomics-based models distinguished cases from controls with high accuracy in this dataset (AUC 0.99). The authors propose that endometriosis may have an under-recognised androgen-dependent component and identify 11-oxygenated androgens as potential diagnostic biomarkers and future therapeutic targets. These findings are promising but preliminary: the proposed blood-based signature requires validation in larger, independent and clinically diverse populations before it could inform diagnosis or treatment.

Review proposing that endometriosis lesions develop through multiple routes: retrograde menstruation, embryonic stem cell remnants, stem cell recruitment, and genetic/epigenetic modifications. Different genetic risk combinations may predispose individuals to different routes of lesion development, contributing to disease heterogeneity. Advocates for molecular profiling and patient-derived organoid models to advance research.

Largest multi-ancestry GWAS and integrated multi-omics study of endometriosis to date, analyzing ~1.4 million women including 105,869 cases. The study identified 80 genomic risk loci, including 37 new loci, and linked risk signals to pathways involved in cell differentiation, immune and hormonal regulation, tissue remodeling, and inflammation. It also found partial genetic overlap with adenomyosis and interactions between polygenic endometriosis risk and symptoms such as abdominal pain, anxiety, migraine, and nausea; these findings are association-based and do not imply deterministic prediction for individual patients.

Review reframing endometriosis as a systemic disorder of distributed network dysregulation rather than a purely pelvic condition. The authors map reciprocal signalling between aberrant sensory nerve growth and dysfunctional immune responses as key events in lesion development and sustained pain. This neuroimmune crosstalk shapes epithelial and stromal behaviour, amplifies inflammation, and reinforces pain circuitry. They propose that targeting key neuroimmune nodes may offer new therapeutic opportunities to curb both lesion progression and endometriosis-related chronic pain.

Preprint study showing elevated transferrin and its receptor in endometriotic cells alongside reduced antioxidant capacity. Experimental knockdown of transferrin suppressed cell proliferation and migration while increasing apoptosis, implicating the transferrin/ferroptosis axis in disease pathogenesis. Findings are preliminary and have not yet undergone peer review.