Li Gao1, Qing Dong1, Zhenghong Song1, Fei Shen1, Jianquan Shi2, Yansheng Li3. 1. Department of Neurology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201100, China. 2. Department of Neurology, Nanjing First Hospital, Nanjing Medical University, Nanjing, 210000, China. 3. Department of Neurology, Ren Ji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 201100, China. lliyans@hotmail.com.
Abstract
BACKGROUND: Recently, several studies have demonstrated that the NLRP3 inflammasome participates in detecting cellular damage and mediating inflammatory responses to aseptic tissue injury following cerebral ischemia. More importantly, blocking or inhibiting NLRP3 inflammasome at multiple levels, such as its expression, assembly and activity, may offer substantial promise to salvage neurological deterioration during ischemic stroke. However, the specific mechanisms about the contribution of NLRP3 to neurovascular damage remain to be established. MATERIALS AND METHODS: In this paper, we will review the molecular structure, expression and assembly of NLRP3 inflammasome, and illustrate its possible roles and effects in ischemic stroke. Moreover, we will speculate its activity and mechanism in stroke pathogenesis, and present the recent advances and challenges in potential therapies targeting NLRP3 inflammsome. RESULTS AND CONCLUSION: Mounting evidence has demonstrated that NLRP3 inflammasome plays a prominent role in the pathogenesis and progression of ischemic stroke, which indicates the higher possibility to target NLRP3 inflammasome in future stroke therapy. However, many aspects of the biology of NLRP3 inflammasome to stroke are still not well defined or even completely unknown. As the mechanistic insight of the NLRP3 inflammasomes increases, opportunities to develop new therapeutic strategies for patients with ischemic stroke are expected to enhance proportionately.
BACKGROUND: Recently, several studies have demonstrated that the NLRP3 inflammasome participates in detecting cellular damage and mediating inflammatory responses to aseptic tissue injury following cerebral ischemia. More importantly, blocking or inhibiting NLRP3 inflammasome at multiple levels, such as its expression, assembly and activity, may offer substantial promise to salvage neurological deterioration during ischemic stroke. However, the specific mechanisms about the contribution of NLRP3 to neurovascular damage remain to be established. MATERIALS AND METHODS: In this paper, we will review the molecular structure, expression and assembly of NLRP3 inflammasome, and illustrate its possible roles and effects in ischemic stroke. Moreover, we will speculate its activity and mechanism in stroke pathogenesis, and present the recent advances and challenges in potential therapies targeting NLRP3 inflammsome. RESULTS AND CONCLUSION: Mounting evidence has demonstrated that NLRP3 inflammasome plays a prominent role in the pathogenesis and progression of ischemic stroke, which indicates the higher possibility to target NLRP3 inflammasome in future stroke therapy. However, many aspects of the biology of NLRP3 inflammasome to stroke are still not well defined or even completely unknown. As the mechanistic insight of the NLRP3 inflammasomes increases, opportunities to develop new therapeutic strategies for patients with ischemic stroke are expected to enhance proportionately.
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