Calpain modulation of programmed cell death pathways following cerebral ischemia

P. S. Vosler, J. Chen

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Cerebral ischemia causes a massive insult resulting in the eventual death of ischemia-affected neurons. Historically, research efforts have focused on the canonical cell death signaling pathways examining the activation of both caspase-dependent and -independent mechanisms to execute neuronal death due to ischemia. Recently, however, there is evidence that the calcium-activated protease calpain is able to mediate both neuronal death pathways. This chapter briefly outlines the intrinsic and extrinsic caspase-dependent pathways and the caspase-independent pathways. This is followed by a discussion of the role of calpain in abrogating the caspase-dependent pathway and instigating the caspase-independent pathway. Greater understanding of how neurons actuate delayed neuronal death will potentially lead to the development of viable therapeutics to diminish the negative neurological sequelae caused by cerebral ischemia.

Original languageEnglish (US)
Title of host publicationExperimental Stroke
PublisherBentham Science Publishers Ltd.
Pages1-8
Number of pages8
ISBN (Print)9781608056668
DOIs
StatePublished - Dec 1 2008
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

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