Extrinsic Pathway

The extrinsic, or mitochondrial-independent cell-death, pathway is initiated by the members of death receptor families. Fas/Fas ligand (FasL) is perhaps the most studied pathway with respect to cerebral ischemia. Following experimental stroke, Fas expression has been described, and blocking this pathway by depleting the brain of FasL appears to reduce brain injury (111 ). This pathway is initiated when the Fas receptor is activated by its corresponding ligand, FasL. Once FasL binds with the Fas receptor, the complex then recruits Fas-associated death domain, a Fas receptor-adaptor protein, from the cytosol and activates caspase-8. Caspase-8 activates caspase-3, leading to DNA damage and cell death in a pathway that is likely identical to the intrinsic pathway. The extrinsic pathway can also interface with the intrinsic pathway, because caspase-8 cleaves Bid, a member of the Bcl-2 family, to form a truncated form (t-Bid), which has the capacity to translocate to the mitochondria and induce cytochrome c release (112).

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