Programmed Cell Death of Endothelial Cells in Myocardial Infarction and Its Potential Therapeutic Strategy

Figure 1

Molecular mechanisms of pyroptosis, apoptosis, and necroptosis and their network interactions. The intrinsic pathway of apoptosis (blue) is induced by the triggering of MOMP by BAX and BAK leading to cytochrome C activation and further activation of caspase-9 on APF1. Death receptor-mediated apoptosis requires the formation of a pro-apoptotic caspase-8 dimer, and both caspase-8 and caspase-9 promote the downstream executioner caspase-3 and caspase-7 activation, which induces apoptosis. Activation of death receptors similarly triggers necroptosis (orange). Activated RIPK3 phosphorylates and activates the executor of necroptosis, MLKL, which forms pores in the cell membrane, leading to cell lysis and the release of DAMPs. Cellular stress leads to inflammasome formation and activation of caspase-1 and cleavage of GSDMD, and cytokines such as IL-18 and IL-1β are released through the membrane pores formed by GSDMD-N and trigger pyroptosis (green).