Fig. 7
Summary of the NEC-induced cell death pathway in full-term and preterm rats. In full-term model rats, FASL-FAS induced pro-caspase-8, which activated caspase-8, caspase-3/7, and PARP1 to promote apoptosis. Furthermore, p53, Bax, and caspase-9 were activated by DNA damage caused by ROS stress. Phosphorylated RIPK3 and MLKL independently induced necrosis. In preterm rats, TNF-α induced apoptosis via caspase-8 activation. TRAF-2, TRADD, RIPK1, FADD, and the pro-caspase-8 family have all been shown to reflect the crosstalk between necrosis and apoptosis via MLKL phosphorylation and the activation of caspase-8, respectively. By inhibiting Bax, Bcl2 overexpression impairs the promotion of Bax and caspase-9.
