粒体自噬
脑病
窒息
医学
细胞生物学
线粒体生物发生
神经科学
缺血
线粒体融合
线粒体
自噬
新生儿窒息
半影
围产期窒息
生物
生理学
生物信息学
MFN2型
麻醉
内科学
线粒体DNA
遗传学
基因
细胞凋亡
作者
Claire Thornton,Adam Jones,Syam Nair,Afra Aabdien,Carina Mallard,Henrik Hagberg
出处
期刊:FEBS Letters
[Wiley]
日期:2017-12-18
卷期号:592 (5): 812-830
被引量:47
标识
DOI:10.1002/1873-3468.12943
摘要
Hypoxic-ischaemic encephalopathy, resulting from asphyxia during birth, affects 2-3 in every 1000 term infants and depending on severity, brings about life-changing neurological consequences or death. This hypoxic-ischaemia (HI) results in a delayed neural energy failure during which the majority of brain injury occurs. Currently, there are limited treatment options and additional therapies are urgently required. Mitochondrial dysfunction acts as a focal point in injury development in the immature brain. Not only do mitochondria become permeabilised, but recent findings implicate perturbations in mitochondrial dynamics (fission, fusion), mitophagy and biogenesis. Mitoprotective therapies may therefore offer a new avenue of intervention for babies who suffer lifelong disabilities due to birth asphyxia.
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