作者: Ruoyang Shi , Jiequn Weng , Paul Szelemej , Jiming Kong
DOI: 10.1007/978-1-4419-9530-8_7
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摘要: Delayed neuronal death in the penumbral region of a stroke is largely responsible for many negative implications seen victims. This type occurs forms, including apoptosis, necrosis, and alternative mechanisms. Although caspases are usually associated with there several morphologically biochemically distinct types cell that independent caspase activation. Downstream effectors processes mitochondrial damage, such as AIF, endonuclease G, BNIP3, mitophagy, biogenesis, chaperone-mediated autophagy, reactive oxygen species production well parallel endoplasmic reticular stress lysosomal dysfunction, have all been shown to play role post-stroke delayed death. In this chapter, we attempt summarize these caspase-independent events their potential therapeutic applications targets intervention.