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Ramsay RR, Rashed MS, Nelson SD

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This suggests potential benefit in limiting early damage but highlights the complexity of translating salvage to reduced final infarct size

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Akt is deactivated and Bcl-2-associated death promoter (BAD) phosphorylation is lost in one pathway due to a stalled survival pathway, whereas Fas cell surface death receptor (FAS) is upregulated through stimulation of c-Jun-N-terminal kinase, which activates caspase-8, phosphorylates Fas-associated protein with death domain (FADD), and truncates BH3-interacting domain death agonist (BID)