期刊
FEBS LETTERS
卷 592, 期 5, 页码 812-830出版社
WILEY
DOI: 10.1002/1873-3468.12943
关键词
biogenesis; brain injury; fission; fusion; mitochondria; mitophagy; neonatal
资金
- UK Medical Research Council [MR/N013700/1]
- King's College London, MRC Doctoral Training Partnership in Biomedical Sciences
- Frimurarna Barnhusdirektionen Foundation
- ERANET (MICRO-MET, EU and research councils in Europe) [VR2014-7551]
- Biochemical Society Summer Fellowship [DCRB170512081]
- Medical Research Council/King's Health Partners [MC_PC_15031]
- SPARKS [15KCL05]
- Swedish Medical Research Council [VR2012-3500, VR 2012-2992]
- ALF-LUA [ALFGBG426401, ALFGBG-432291]
- Swedish Brain Foundation [FO2015-0094, FO2015-0190]
- Byggmastare Olle Engkvist Foundation
- Wilhelm & Martina Lundgren Foundation
- Ahlen Foundation
- Torsten Soderberg Foundation [M98/15]
- MRC [1935843, MC_PC_15031] Funding Source: UKRI
- Medical Research Council [MC_PC_15031] Funding Source: researchfish
- Action Medical Research [2485] Funding Source: researchfish
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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