Transcriptomic profiling of G3BP2 lesion-specific knockout in a mouse model of endometriosis
Endometriosis is a chronic estrogen-dependent disorder characterized by the growth of ectopic endometrial tissue and a high rate of recurrence, yet the molecular mechanisms that support lesion survival and metabolic adaptation remain incompletely understood. In this study, we performed transcriptomic profiling of ectopic endometriotic lesions isolated from a mouse model with lesion-specific deletion of G3bp2, alongside matched control lesions. By comparing gene expression programs between G3bp2-deficient and control ectopic lesions, this dataset aims to define the transcriptional pathways regulated by G3BP2 in the local lesion microenvironment. These data provide a resource for investigating lesion-intrinsic regulatory mechanisms in endometriosis and may facilitate the identification of molecular pathways relevant to ectopic lesion maintenance and therapeutic targeting.