雌激素和铁调素在缺血性脑卒中后调控铁死亡的作用

The role of estrogen and hepcidin in regulating ferroptosis after ischemic stroke

缺血性脑卒中诱发的一系列病理生理反应导致神经细胞死亡。铁死亡作为一种新发现的细胞死亡类型,也被发现存在于中枢神经系统中。铁死亡的触发与铁代谢密切相关,在调节铁代谢的过程中铁调素起关键作用。缺血后小胶质细胞活化与极化,产生大量的炎症因子,诱导中枢神经系统铁调素高表达,从而破坏神经细胞铁稳态。因此,干预铁调素的表达与作用,是抑制脑缺血后神经元铁死亡的重要措施。有研究发现,雌激素在中枢神经系统中可降低铁沉积,维持脑内铁稳态。本文讨论了脑缺血发生后神经元的铁死亡以及神经系统中铁调素、雌激素的作用,为缺血性脑卒中的治疗提供了新思路。

A series of pathophysiological reactions induced by ischemic stroke lead to nerve cell death.Ferroptosis,as a newly discovered type of cell death,has also been found to exist in the central nervous system(CNS).The trigger of ferroptosis is closely related to iron metabolism,In the process of regulating iron metabolism,hepcidin plays a key role.After ischemia,microglia are activated and polarized to produce a large number of inflammatory factors,which induces high expression of hepcidin in the CNS,thereby destroying the iron homeostasis of neurons.Therefore,intervention in the expression and effect of hepcidin is an important target to inhibit ferroptosis of neurons after cerebral ischemia.Studies have found that estrogen in the CNS can reduce iron deposition and maintain iron homeostasis in the brain.This review discusses the ferroptosis of neurons after cerebral ischemia,the role of hepcidin and estrogen in the CNS on ischemic condition,providing a new idea for the treatment of ischemic stroke.