缺血性卒中后神经元的泛素化调控

Ubiquitination Regulation of Neurons after Ischemic Stroke

缺血性卒中所致严重脑损伤是世界范围内死亡和致残的主要原因之一,神经元损伤一直是缺血性卒中后一系列复杂分子机制的研究热点。泛素化是以多种细胞蛋白为降解目标的翻译后蛋白质修饰,受到严格的调控,对于细胞存活至关重要。泛素化与多种神经系统疾病的发生、发展息息相关,许多神经系统疾病都表现出泛素化蛋白的聚集;同时神经元易受到蛋白质组成变化的影响,泛素化修饰成为缺血性卒中后神经元存活和损伤的重要翻译后机制,神经元泛素稳态的失衡可能是导致缺血性卒中损伤的重要因素。

Ischemic stroke leads to serious brain injury,which is one of the main causes of death and disability in the world.Neuronal damage has been a hot research topic in a series of complex molecular mechanisms after ischemic stroke.Ubiquitination is a kind of post-translational protein modification with multiple cellular proteins as degradation targets,which is strictly regulated and essential for the cell survival.Ubiquitination is closely related to the occurrence and development of a variety of nervous system diseases,and many nervous system diseases show the aggregation of ubiquitination proteins.At the same time,neurons are very vulnerable to changes in protein composition,therefore ubiquitination is an important post-translational mechanism for neuronal survival and injury after cerebral ischemia,and the imbalance of neuron ubiquitin homeostasis may be an important factor leading to ischemic stroke injury.