Regulated cell death in hypoxic-ischaemic encephalopathy: recent development and mechanistic overview

被引:4
作者
Wu, Lingzhi [1 ]
Chang, Enqiang [1 ]
Zhao, Hailin [1 ]
Ma, Daqing [1 ,2 ]
机构
[1] Imperial Coll London, Chelsea & Westminster Hosp, Fac Med, Div Anaesthet Pain Med & Intens Care,Dept Surg & C, London, England
[2] Zhejiang Univ, Childrens Hosp, Natl Clin Res Ctr Child Hlth, Perioperat & Syst Med Lab,Sch Med, Hangzhou 310052, Peoples R China
关键词
NLRP3 INFLAMMASOME ACTIVATION; MIXED LINEAGE KINASE; BRAIN-INJURY; CEREBRAL-ISCHEMIA; GASDERMIN D; NEURON DEATH; RIP1; KINASE; K+ EFFLUX; PROTEIN; FERROPTOSIS;
D O I
10.1038/s41420-024-02014-2
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Hypoxic-ischaemic encephalopathy (HIE) in termed infants remains a significant cause of morbidity and mortality worldwide despite the introduction of therapeutic hypothermia. Depending on the cell type, cellular context, metabolic predisposition and insult severity, cell death in the injured immature brain can be highly heterogenous. A continuum of cell death exists in the H/I-injured immature brain. Aside from apoptosis, emerging evidence supports the pathological activation of necroptosis, pyroptosis and ferroptosis as alternative regulated cell death (RCD) in HIE to trigger neuroinflammation and metabolic disturbances in addition to cell loss. Upregulation of autophagy and mitophagy in HIE represents an intrinsic neuroprotective strategy. Molecular crosstalk between RCD pathways implies one RCD mechanism may compensate for the loss of function of another. Moreover, mitochondrion was identified as the signalling "hub" where different RCD pathways converge. The highly-orchestrated nature of RCD makes them promising therapeutic targets. Better understanding of RCD mechanisms and crosstalk between RCD subtypes likely shed light on novel therapy development for HIE. The identification of a potential RCD converging node may open up the opportunity for simultaneous and synergistic inhibition of cell death in the immature brain.
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页数:16
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