内质网应激在热射病脑损伤中的研究进展

Research progress of endoplasmic reticulum stress in cerebral injury induced by heat stroke

热射病是一种危及生命的全身性疾病,其特征是核心体温升高超过40℃,并伴有中枢神经系统功能障碍及出现多器官功能障碍综合征。热射病引起的中枢系统损伤即脑损伤其突出表现为神经炎症,而内质网应激是导致神经炎症的重要机制之一。内质网应激通过IRE1α、PERK和ATF6等信号通路调节蛋白质折叠和细胞稳态,这些通路在热射病中的异常激活可能导致细胞凋亡和脑损伤。研究发现,热射病模型中内质网应激相关蛋白表达增加,表明内质网应激在热射病脑损伤中起关键作用。尽管具体机制尚待进一步研究,但内质网应激相关通路的深入研究有望为热射病脑损伤的治疗提供新的思路。

heat stroke is a potentially fatal systemic condition characterized by a core body temperature exceeding 40℃,central nervous system dysfunction,and the onset of multiple organ dysfunction syndrome.Heat stroke-induced central nervous system injury,is prominently manifested as neuroinflammation,with endoplasmic reticulum stress playing a pivotal role in neuroinflammation development.The endoplasmic reticulum stress regulates protein folding and cellular homeostasis through signaling pathways,such as IRE1α,PERK,and ATF6.Abnormal activation of these pathways in heat stroke may lead to cell apoptosis and cerebral injury.Studies have shown an increase in ERS-related protein expression in heat stroke models,indicating its pivotal role in heat stroke-induced cerebral injury.Although the specific mechanism is still under investigation,further research on ERS-related pathways may offer new insights into the treatment of heat stroke-induced cerebral injury.