Neuroinflammation is a complex inflammatory response of the nervous system that may be triggered by various pathogens or toxins and induces immunocyte infiltration and activation. Recently, cell death has been shown to play a key role in mediating neuroinflammation. Apoptosis has long been considered the only type of programmed cell death (PCD) until a range of cell deaths, both PCD and non-PCD, have been demonstrated, such as necroptosis, pyroptosis, ferroptosis, autophagy-associated cell death and oxeiptosis. Cell death leads to the “rupture” of the plasma membrane and the subsequent release of intracellular contents, which promotes a pro-inflammatory response of the immune system into the surrounding microenvironment.
Neuroinflammatory response is considered to be a key factor in nervous system diseases such as multiple sclerosis, Alzheimer's disease and glaucoma. For example, the activation of NLRP3/NLRP6 /caspase-1 is recruited to cleave GSDMD, which characterized microglial pyroptosis. Meanwhile, on the inflammasome platform, mature forms of IL-1ß and IL-18 are managed, which mediates pyroptosis to exert neurotoxicity for retinal ganglion cells. There is growing evidence that targeting unique cell death pathways can be effective in reducing neuroinflammation and achieving neuroprotection.
In this Research Topic, we discuss the effects of various cell death on inflammatory immune activation, especially focusing on neuroinflammation. We also welcome studies related to the development of novel therapeutics for neuroinflammation by targeting cell death. This Research Topic aims to provide a comprehensive presentation related to molecular dissection and translational investigation of both neuroinflammation and its co-regulation with metabolism and epigenetics. We welcome the submission of Original Research, Methods, Review and Mini-Review articles that cover, but are not limited to, the following topics:
• New molecular mechanisms of immune responses in cell death including apoptosis, necroptosis, pyroptosis, ferroptosis, oxeiptosis and PANoptosis;
• Mechanisms of how the extracellular stimuli such as ischemia/reperfusion were sensed and transduced to initiate neuroinflammation and cell death;
• Crosstalk of cell death with other signaling pathways, metabolic and epigenetic factors at both immunocytes-mediated and nuclear transcriptional factor-mediated levels;
• Cellular protective signaling pathways that contribute to cellular repair during neuroinflammation and the potential interplay between these pathways;
• New strategies to prevent or treat cellular damage in acute or chronic neuroinflammation and autoimmune disease by targeting cell death;
• Translational research for the treatment or prevention of human neuroinflammation diseases targeting unique cell death pathways.
Neuroinflammation is a complex inflammatory response of the nervous system that may be triggered by various pathogens or toxins and induces immunocyte infiltration and activation. Recently, cell death has been shown to play a key role in mediating neuroinflammation. Apoptosis has long been considered the only type of programmed cell death (PCD) until a range of cell deaths, both PCD and non-PCD, have been demonstrated, such as necroptosis, pyroptosis, ferroptosis, autophagy-associated cell death and oxeiptosis. Cell death leads to the “rupture” of the plasma membrane and the subsequent release of intracellular contents, which promotes a pro-inflammatory response of the immune system into the surrounding microenvironment.
Neuroinflammatory response is considered to be a key factor in nervous system diseases such as multiple sclerosis, Alzheimer's disease and glaucoma. For example, the activation of NLRP3/NLRP6 /caspase-1 is recruited to cleave GSDMD, which characterized microglial pyroptosis. Meanwhile, on the inflammasome platform, mature forms of IL-1ß and IL-18 are managed, which mediates pyroptosis to exert neurotoxicity for retinal ganglion cells. There is growing evidence that targeting unique cell death pathways can be effective in reducing neuroinflammation and achieving neuroprotection.
In this Research Topic, we discuss the effects of various cell death on inflammatory immune activation, especially focusing on neuroinflammation. We also welcome studies related to the development of novel therapeutics for neuroinflammation by targeting cell death. This Research Topic aims to provide a comprehensive presentation related to molecular dissection and translational investigation of both neuroinflammation and its co-regulation with metabolism and epigenetics. We welcome the submission of Original Research, Methods, Review and Mini-Review articles that cover, but are not limited to, the following topics:
• New molecular mechanisms of immune responses in cell death including apoptosis, necroptosis, pyroptosis, ferroptosis, oxeiptosis and PANoptosis;
• Mechanisms of how the extracellular stimuli such as ischemia/reperfusion were sensed and transduced to initiate neuroinflammation and cell death;
• Crosstalk of cell death with other signaling pathways, metabolic and epigenetic factors at both immunocytes-mediated and nuclear transcriptional factor-mediated levels;
• Cellular protective signaling pathways that contribute to cellular repair during neuroinflammation and the potential interplay between these pathways;
• New strategies to prevent or treat cellular damage in acute or chronic neuroinflammation and autoimmune disease by targeting cell death;
• Translational research for the treatment or prevention of human neuroinflammation diseases targeting unique cell death pathways.
