Hypoxic-ischemic encephalopathy induces secondary brain injury characterized by delayed energy failure and excitotoxicity.
Hypoxia-ischemia triggers accumulation of reactive oxygen species andintracellular calcium, which induces mitochondrial dysfunction.
Mitochondrial impairment can cause Bax-dependent mitochondrial permeabilization, which triggers release of pro-apoptotic proteins and cell death.
During the recovery phase, Inflammation is produced leading to death receptor activation and induction of necroptosis.