
硫酸软骨素蛋白聚糖对早产儿脑白质损伤后轴突生长抑制作用及机制的研究进展
Research advances in the inhibitory effect of chondroitin sulfate proteoglycans on axon growth after premature white matter injury and its underlying mechanisms
脑白质损伤(white matter injury, WMI)是早产儿脑损伤的重要形式,其典型病理改变主要为少突胶质前体细胞发育障碍及轴突结构损伤,可遗留运动、行为和认知功能障碍等神经系统后遗症。硫酸软骨素蛋白聚糖(chondroitin sulfate proteoglycans, CSPGs)作为细胞外基质重要成分,可通过调控特定受体及信号通路,参与小胶质细胞介导的神经炎症反应,动态平衡胶质瘢痕重构与轴突生长过程。该文就CSPGs与WMI的关系,以及其抑制轴突生长的机制进行综述,并聚焦于多靶点调控CSPGs在促进轴突可塑性和脑功能恢复中的作用,为改善早产儿WMI预后提供理论依据。
White matter injury (WMI) is a major form of brain injury in preterm infants. Its characteristic pathological features primarily involve impaired development of oligodendrocyte precursor cells and structural damage to axons, which can lead to the neurological sequelae such as motor, behavioral, and cognitive dysfunctions. Chondroitin sulfate proteoglycans (CSPGs), as the important components of extracellular matrix, can participate in neuroinflammatory response mediated by microglial cells and dynamically balance glial scar reconstruction and axon growth by regulating specific receptors and signaling pathways. This article reviews the relationship between CSPGs and WMI, as well as the mechanisms by which CSPGs inhibit axon growth, focusing on the role of multi-target regulation of CSPGs in promoting axon plasticity and functional brain recovery, thereby providing a theoretical basis for improving the prognosis of preterm infants with WMI.
脑白质损伤 / 硫酸软骨素蛋白聚糖 / 轴突 / 缺氧缺血 / 早产儿
White matter injury / Chondroitin sulfate proteoglycan / Axon / Hypoxia ischemia / Preterm infant
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所有作者均声明无利益冲突。