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Fibrosis contributes to key pathological features of endometriosis, like pain, adhesions, and organ dysfunction [26]

In vitro studies showed that DHEA and DHEA-S accelerated dermal fibroblast migration (Stevenson et al., 2009) and prevented keratinocyte apoptosis via membrane binding sites (Alexaki et al., 2009), and these processes were reversed when inhibitors of conversion enzymes (aromatase or STS) were used, confirming that conversion to estrogen is required (Pomari et al., 2015)