Fig. 3

Potential effects of HDACs and HDAC inhibitors (HDACis) observed in endometrial pathologies to date. HDACs and HDAC inhibition with HDACis influence the endometrium either directly or indirectly. Several HDACs are differentially expressed in endometrial carcinomas [85, 103]. Inhibition of HDAC2 by valproate induces endometrial cell differentiation [80]. Studies in endometrial carcinoma cells in vitro imply that progesterone through PR induces cell differentiation, while HDACi LBH589 increases PR expression in endometrial cells [101, 102].; SIRT6 induces apoptosis by acting on survivin [103]; TSA and apicidin treatment increase P21 expression, while apicidin alone induces cell cycle arrest by reducing cyclin D1 and CDK4 expression [81, 98]. Cell cycle arrest can also be caused by Vorinostat, Romidepsin, and LBH589 (99–101). HDAC1 and 2 expression levels are upregulated in endometriosis in vitro [8]. and inhibition of SIRT1 can trigger inflammatory response in endometriotic stromal cells [105]. Inhibition of HDACs with TSA induce decidualisation in stromal cells while controlling trophoblast invasion, in vitro [91, 95]. (Created with BioRender.com)