Mechanisms of calpain proteolysis following traumatic brain injury: implications for pathology and therapy: implications for pathology and therapy: a review and update.

Abstract:

:Much recent research has focused on the pathological significance of calcium accumulation in the central nervous system (CNS) following cerebral ischemia, spinal cord injury (SCI), and traumatic brain injury (TBI). Disturbances in neuronal calcium homeostasis may result in the activation of several calcium-sensitive enzymes, including lipases, kinases, phosphatases, and proteases. One potential pathogenic event in a number of acute CNS insults, including TBI, is the activation of the calpains, calcium-activated intracellular proteases. This article reviews new evidence indicating that overactivation of calpains plays a major role in the neurodegenerative cascade following TBI in vivo. Further, this article presents an overview from in vivo and in vitro models of CNS injuries suggesting that administration of calpain inhibitors during the initial 24-h period following injury can attenuate injury-induced derangements of neuronal structure and function. Lastly, this review addresses the potential contribution of other proteases to neuronal damage following TBI.

journal_name

J Neurotrauma

journal_title

Journal of neurotrauma

authors

Kampfl A,Posmantur RM,Zhao X,Schmutzhard E,Clifton GL,Hayes RL

doi

10.1089/neu.1997.14.121

subject

Has Abstract

pub_date

1997-03-01 00:00:00

pages

121-34

issue

3

eissn

0897-7151

issn

1557-9042

journal_volume

14

pub_type

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