TY - JOUR
PY - 2020//
TI - Role of pyroptosis in traumatic brain and spinal cord injuries
JO - International journal of biological sciences
A1 - Hu, Xinli
A1 - Chen, Huanwen
A1 - Xu, Hui
A1 - Wu, Yaosen
A1 - Wu, Chenyu
A1 - Jia, Chang
A1 - Li, Yao
A1 - Sheng, Sunren
A1 - Xu, Cong
A1 - Xu, Huazi
A1 - Ni, Wenfei
A1 - Zhou, Kailiang
SP - 2042
EP - 2050
VL - 16
IS - 12
N2 - Central nervous system (CNS) trauma, including traumatic brain injury (TBI) and spinal cord injury (SCI), remains a leading cause for morbidity and mortality worldwide. Past research has shown that cell death plays a critical role in the pathophysiology of CNS injuries. More recently, pyroptosis has been identified as a form of programmed inflammatory cell death, and it is a unique form of cell death in various aspects. Mechanistically, pyroptosis can be categorized into canonical (mediated by caspase-1) and non-canonical (mediated by caspase-4/5/11). In canonical pyroptosis, Nod-like receptors (NLRs) inflammasomes play a critical role, and their activation promotes the maturation and secretion of the inflammatory cytokines interleukin-1β/18 (IL-1β/18), cleavage of gasdermin D (GSDMD), and ultimately pyroptotic cell death. Despite a plethora of new knowledge regarding pyroptosis, detailed understanding of how pyroptosis is involved in CNS injuries and possible ways to improve clinical outcomes following CNS injuries remain elusive. This review discusses the current knowledge on how pyroptosis is involved in CNS injuries, focusing on new discoveries regarding how pyroptosis activation occurs, differences between CNS cell types following injury, time-course of inflammatory responses, and key regulatory steps of pyroptosis. In addition, we highlight various investigational agents that are capable of regulating key steps in pyroptotic cell death, and we discuss how these agents may be used as therapies to improve outcomes following CNS trauma. Language: en
LA - en
SN - 1449-2288
UR - http://dx.doi.org/10.7150/ijbs.45467
ID - ref1
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