Fig. 7

A disease model for endometriosis. Defective endometrial stromal cell decidualization may be driven by multiple factors including inflammation, chronic endometritis, stress, and/or progesterone resistance. This, in turn, may direct stromal cell differentiation in the direction of chronic inflammation and senescence, with accompanying senescence-associated secretory phenotypes (SASPs), which include pro-inflammatory mediators and proteases. The senescence phenotype may also impair decidualization. Reduced decidualization may also compromise the infiltration and proliferation of uNK cells, which are likely to be important for senescent cell removal. Further analysis of other cells in menstrual effluent will be important to provide further support for this model