I work in Roser Vento-Tormo’s group in the Cellular Genetics Programme at Sanger. This group has helped contribute to the field in recent years by generating comprehensive single-cell atlases of the endometrium.14,15 The atlases show how individual cells behave and change in different parts of the body (spatial) and over time (temporal). The endometrium is a highly dynamic tissue, consisting of two main compartments: epithelial, which are made up of cells that line surfaces, and stromal, which provide support and structure. Fibroblasts (a fibrous material making up connective tissue), immune cells and blood vessels populate the stromal compartment, and through signalling interactions with the epithelium, they regulate the proliferation and destruction of the whole endometrium during the menstrual cycle.5
Part of this work has identified macrophages in the uterus as key players in the process of endometrial proliferation – the renewal of the endometrium after menstruation.14 Furthermore, we have also identified key differences in these macrophages between healthy people and patients with endometriosis. Plus we’ve found an endometriosis-specific signature – a specific pattern of gene activity – in stromal fibroblasts, which might impair normal differentiation of the endometrium. This work was possible due to the large repository of tissue samples collected from both healthy individuals and those with endometriosis.14,15
In parallel, these tissue samples are also contributing to an ever-expanding biobank of organoids from the endometrium of both healthy individuals and endometriosis patients, with organoids being generated directly from endometriosis lesions. These in vitro organoid models can contribute to our understanding of endometriosis by allowing specific biological questions and changes to be studied at multiple time points and at a large scale that cannot be done in real patients.