SENP1参与慢性间歇低氧小胶质细胞极化及神经元损伤机制的研究进展

Research Progress of Mechanism of SENP1 in Polarization of Microglia and Neuronal Injury in Chronic Intermittent Hypoxia

慢性间歇低氧(CIH)诱导的中枢神经系统(CNS)炎症反应是阻塞性睡眠呼吸暂停低通气综合征(OSAHS)神经认知功能障碍最重要的病理机制之一。小胶质细胞是维持CNS内环境稳定最重要的免疫反应细胞,不同的极化状态对神经元细胞产生损害或保护作用,准确调控小胶质细胞极化状态是控制炎症反应的关键,有助于维持神经认知功能正常。小类泛素相关修饰物(SUMO)修饰广泛参与机体蛋白翻译后修饰,SUMO特异性蛋白酶1是一种关键的去SUMO化蛋白酶,两者可能参与小胶质细胞极化状态、CNS炎症反应及神经元损伤或凋亡的调控。因此,深入了解CIH小胶质细胞极化及炎症反应机制,能为防治OSAHS神经认知功能障碍提供新思路。

Inflammatory reaction of central nervous system(CNS)induced by chronic intermittent hypoxia(CIH)is one of the most important pathological mechanisms of neurocognitive dysfunction in obstructive sleep apnea hypopnea syndrome(OSAHS).Microglia cells are the most important immune response cells to maintain the stability of the internal environment of CNS.Different polarization states have damaging or protective effects on neuron cells.Accurate regulation of microglia polarization state is the key to control inflammatory response and maintain normal neurocognitive function.Small ubiquitin-related modifier(SUMO)is widely involved in post-translational modification of body proteins.SUMO specific proteases 1 is a key desumoylation protease,which both may participate in the polarization state of microglia cells,the inflammatory response of CNS,and the regulation of neuron injury or apoptosis.Therefore,further understanding of the polarization of microglia cells and inflammatory response mechanism in CIH can offer new ideas to prevent and treat OSAHS neurocognitive dysfunction.