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Inflammasome: Its role in traumatic brain and spinal cord injury

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

  1. RWTH Aachen University, Aachen, Germany
  2. Kurdistan University of Medical Sciences, Sanandaj, Iran
  3. Tehran University of Medical Sciences, Tehran, Iran

向作者/读者索取更多资源

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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