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lüll Apoptotic mechanisms after cerebral ischemia Broughton BR; Reutens DC; Sobey CGStroke 2009[May]; 40 (5): e331-9BACKGROUND AND PURPOSE: Traditionally, cell death after cerebral ischemia was considered to be exclusively necrotic in nature, but research over the past decade has revealed that after a stroke, many neurons in the ischemic penumbra will undergo apoptosis. SUMMARY OF REVIEW: This brief review provides a general overview and update of various signaling pathways in the development of apoptosis in ischemic lesions. Cerebral ischemia triggers two general pathways of apoptosis: the intrinsic pathway, originating from mitochondrial release of cytochrome c and associated stimulation of caspase-3; and the extrinsic pathway, originating from the activation of cell surface death receptors, resulting in the stimulation of caspase-8. Although many of the key apoptotic proteins have been identified, our understanding of the complex underlying mechanisms remains poor and hence treatment of stroke patients by manipulating apoptotic pathways remains a daunting task. However, recent advances in the field have helped broaden our knowledge of apoptosis after cerebral ischemia. Further to the simplistic concept that stroke-induced apoptosis occurs predominantly in neurons and is caspase-dependent, accumulating evidence now indicates that apoptosis is prevalent in nonneuronal cells and that caspase-independent mechanisms also play a key role. CONCLUSIONS: Although the ischemic penumbra is under threat of infarction, it is potentially salvageable and thus represents an opportunity for therapeutic intervention.|Animals[MESH]|Apoptosis Regulatory Proteins/physiology[MESH]|Apoptosis/*physiology[MESH]|Brain Ischemia/*pathology[MESH]|Calcium Channels/metabolism[MESH]|Calcium/metabolism[MESH]|Caspases/physiology[MESH]|DNA Damage[MESH]|Humans[MESH]|Reactive Oxygen Species/metabolism[MESH]|Receptors, Tumor Necrosis Factor/physiology[MESH]|fas Receptor/physiology[MESH] |