期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 233, 期 7, 页码 5160-5169出版社
WILEY
DOI: 10.1002/jcp.26287
关键词
caspase-1; inflammasomes; interleukin-1 (IL-1); NLRP1; NLRP3; spinal cord injury (SCI); traumatic brain injury (TBI)
资金
- RWTH Aachen University, Aachen, Germany
- Kurdistan University of Medical Sciences, Sanandaj, Iran
- Tehran University of Medical Sciences, Tehran, Iran
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-1). 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).
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