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Abstract：
BACKGROUND: Currently, spinal cord injury (SCI) is a pathological incident that triggers several neuropathological conditions, leading to the initiation of neuronal damage with several pro-inflammatory mediators\' release. However, pyroptosis is recognized as a new programmed cell death mechanism regulated by the stimulation of caspase-1 and/or caspase-11/-4/-5 signaling pathways with a series of inflammatory responses.
OBJECTIVE: Our current review concisely summarizes the potential role of pyroptosis-regulated programmed cell death in SCI, according to several molecular and pathophysiological mechanisms. This review also highlights the targeting of pyroptosis signaling pathways and inflammasome components and its therapeutic implications for the treatment of SCI.
UNASSIGNED: Multiple pieces of evidence have illustrated that pyroptosis plays significant roles in cell swelling, plasma membrane lysis, chromatin fragmentation and intracellular pro-inflammatory factors including IL-18 and IL-1β release. In addition, pyroptosis is directly mediated by the recently discovered family of pore-forming protein known as GSDMD. Current investigations have documented that pyroptosis-regulated cell death plays a critical role in the pathogenesis of multiple neurological disorders as well as SCI. Our narrative article suggests that inhibiting the pyroptosis-regulated cell death and inflammasome components could be a promising therapeutic approach for the treatment of SCI in the near future.
OBJECTIVE: Our current review concisely summarizes the potential role of pyroptosis-regulated programmed cell death in SCI, according to several molecular and pathophysiological mechanisms. This review also highlights the targeting of pyroptosis signaling pathways and inflammasome components and its therapeutic implications for the treatment of SCI.
UNASSIGNED: Multiple pieces of evidence have illustrated that pyroptosis plays significant roles in cell swelling, plasma membrane lysis, chromatin fragmentation and intracellular pro-inflammatory factors including IL-18 and IL-1β release. In addition, pyroptosis is directly mediated by the recently discovered family of pore-forming protein known as GSDMD. Current investigations have documented that pyroptosis-regulated cell death plays a critical role in the pathogenesis of multiple neurological disorders as well as SCI. Our narrative article suggests that inhibiting the pyroptosis-regulated cell death and inflammasome components could be a promising therapeutic approach for the treatment of SCI in the near future.
摘要：
背景：目前，脊髓损伤（SCI）是一种病理事件，会引发多种神经病理学状况，通过几种促炎介质释放导致神经元损伤的开始。然而,焦亡被认为是一种新的程序性细胞死亡机制，受caspase-1和/或caspase-11/-4/-5信号通路刺激的一系列炎症反应调控。
目的：我们当前的综述根据几种分子和病理生理机制，简要总结了在SCI中焦凋亡调节的程序性细胞死亡的潜在作用。这篇综述还强调了焦凋亡信号通路和炎性小体成分的靶向及其对SCI治疗的治疗意义。
■多个证据表明，焦亡在细胞肿胀中起着重要作用，质膜裂解，染色质碎片和细胞内促炎因子，包括IL-18和IL-1β释放。此外,焦亡是由最近发现的称为GSDMD的成孔蛋白家族直接介导的。目前的研究表明，焦凋亡调节的细胞死亡在多种神经系统疾病以及SCI的发病机理中起着至关重要的作用。我们的叙述文章表明，在不久的将来，抑制焦凋亡调节的细胞死亡和炎症小体成分可能是治疗SCI的有希望的治疗方法。
目的：我们当前的综述根据几种分子和病理生理机制，简要总结了在SCI中焦凋亡调节的程序性细胞死亡的潜在作用。这篇综述还强调了焦凋亡信号通路和炎性小体成分的靶向及其对SCI治疗的治疗意义。
■多个证据表明，焦亡在细胞肿胀中起着重要作用，质膜裂解，染色质碎片和细胞内促炎因子，包括IL-18和IL-1β释放。此外,焦亡是由最近发现的称为GSDMD的成孔蛋白家族直接介导的。目前的研究表明，焦凋亡调节的细胞死亡在多种神经系统疾病以及SCI的发病机理中起着至关重要的作用。我们的叙述文章表明，在不久的将来，抑制焦凋亡调节的细胞死亡和炎症小体成分可能是治疗SCI的有希望的治疗方法。
