Citation

Mortezaee K, Khanlarkhani N, Beyer C, Zendedel A. J. Cell. Physiol. 2018; 233(7): 5160-5169.

Affiliation

Institute of Neuroanatomy, School of Medicine, RWTH Aachen University, 52074 Aachen, Germany.

Copyright

(Copyright © 2018, Wistar Institute of Anatomy and Biology)

DOI

10.1002/jcp.26287

PMID

29150951

Abstract

Traumatic brain injury (TBI) and spinal cord injury (SCI) are pathological events that lead to neuropathological conditions which have in consequence the initiation of pro-inflammatory cytokine production. Neuroinflammation plays a key role in the secondary phase of both TBI and SCI after initial cell death. Activation of cytoplasmic inflammasome complexes is regarded as the essential step of neuroinflammation and a key trigger for neuronal death called pyroptosis. Inflammasome complexes are involved in activation of caspase-1 which catalyzes the cleavage of pro-interleukins into their active forms (including interleukin-18 (IL-18) and IL-1β). The focus of this article is to discuss the time-course and regulation of inflammasome assembly and activation during TBI and SCI and their targeting in designing therapeutic approaches. We particularly focus on the inflammasomes NLRP1 and NLRP3 which play a pivotal function during TBI and SCI in the central nervous system (CNS). This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.

Language: en

Keywords

NLRP1; NLRP3; Traumatic brain injury (TBI); caspase-1; inflammasomes; interleukin-1β (IL-1β); spinal cord injury (SCI)