线粒体在新生儿缺氧缺血性脑损伤机制中作用的研究进展

Research progress on the role of mitochondria in the mechanism of neonatal hypoxicischemic brain damage

新生儿缺氧缺血性脑损伤是引起新生儿早期死亡和远期神经障碍的主要原因之一,它主要是由缺氧以及脑血流受限造成的。新生儿缺氧缺血性脑损伤机制复杂,主要与氧化应激、神经炎症以及神经兴奋性毒性有关,而线粒体参与了该机制的发展过程。近年来,线粒体功能障碍是未成熟脑损伤发生发展的研究焦点。主要表现为线粒体形态结构异常、功能及动力学的改变。本文就缺氧缺血性脑损伤后线粒体的形态、功能和动力学的改变以及针对线粒体的干预治疗策略进行综述,从而为新生儿缺氧缺血性脑损伤治疗的新方向提供理论依据。

Neonatal hypoxic-ischemic brain damage is a leading cause of early neonatal mortality and long-term neurological disorders,primarily resulting from hypoxia and restricted cerebral blood flow.The mechanisms involved in neonatal hypoxic-ischemic brain injury are complex,involving oxidative stress,neuroinflammation,and excitotoxicity,with mitochondria playing a pivotal role in these processes.In recent years,mitochondrial dysfunction has emerged as a key factor in the development and progression of immature brain injury,characterized by abnormalities in mitochondrial morphology,function,and dynamics.This study reviewed the alterations in mitochondrial morphology,function,and dynamics post hypoxicischemic brain injury,along with potential mitochondrial intervention strategies,offering a theoretical foundation for novel therapy approaches for treating neonatal hypoxic-ischemic brain injury.