Li Wen-Xing, Qu Yi, Mu De-Zhi, Tang Jun
Department of Pediatrics, West China Second Hospital, Sichuan University/Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Chengdu 610041, China.
Zhongguo Dang Dai Er Ke Za Zhi. 2018 Oct;20(10):864-869. doi: 10.7499/j.issn.1008-8830.2018.10.017.
White matter injury in preterm infants has a complex etiology and can lead to long-term neurocognitive and behavioral deficits, but there are still no specific treatment methods for this disease at present. More and more studies have shown that mitochondrial dysfunction plays an important role in the pathogenesis of white matter injury in preterm infants and might be a common subcellular mechanism of white matter developmental disorder, which involves oxidative stress, reduced ATP synthesis, and disequilibrium of calcium homeostasis. This article reviews the role of mitochondria in brain development and the mechanism of mitochondrial dysfunction, with a hope to perform early intervention of white matter injury in preterm infants by protecting mitochondrial function, so as to provide a reference for improving the neurodevelopmental outcome of preterm infants who survive.
早产儿脑白质损伤病因复杂，可导致长期神经认知和行为缺陷，但目前针对该疾病仍无特效治疗方法。越来越多的研究表明，线粒体功能障碍在早产儿脑白质损伤发病机制中起重要作用，可能是脑白质发育障碍的共同亚细胞机制，涉及氧化应激、ATP合成减少和钙稳态失衡。本文综述线粒体在脑发育中的作用及线粒体功能障碍机制，以期通过保护线粒体功能对早产儿脑白质损伤进行早期干预，为改善存活早产儿神经发育结局提供参考。
