Fig. 1

A proposed model depicting the possible mechanism underlying hydrogen/GSDMD- mediated cell pyroptosis in endometrial cancer. Hydrogen triggers the activation of ROS/NLPR3 signaling, which enables caspase-1 activation. GSDMD is cleaved off the suppressor C-terminal domain of the protein and liberates the pore-forming N-terminal domain of GSDMD, which then self-assembles to form pores in the plasma membrane that we call “hydrogen channels.” This then regulates the precursor of the proinflammatory cytokine IL-1β into its active form, mature IL-1β. These inflammatory genes constitute an inflammatory microenvironment in which to modulate cellular pyroptosis