References
[1] Back SA. White matter injury in the preterm infant:pathology and mechanisms[J]. Acta Neuropathol, 2017, 134(3):331-349.
[2] Cree BAC, Niu J, Hoi KK, et al. Clemastine rescues myelination defects and promotes functional recovery in hypoxic brain injury[J]. Brain, 2018, 141(1):85-98.
[3] Bonora M, De Marchi E, Patergnani S, et al. Tumor necrosis factor-α impairs oligodendroglial differentiation through a mitochondria-dependent process[J]. Cell Death Differ, 2014, 21(8):1198-1208.
[4] Back SA, Luo NL, Borenstein NS, et al. Late oligodendrocyte progenitors coincide with the developmental window of vulnerability for human perinatal white matter injury[J]. J Neurosci, 2001, 21(4):1302-1312.
[5] Kim HJ, Shaker MR, Cho B, et al. Dynamin-related protein 1 controls the migration and neuronal differentiation of subventricular zone-derived neural progenitor cells[J]. Sci Rep, 2015, 5:15962.
[6] Erecinska M, Cherian S, Silver IA. Energy metabolism in mammalian brain during development[J]. Prog Neurobiol, 2004, 73(6):397-445.
[7] Kostić MM, Zivković RV, Rapoport SM. Maturation-dependent changes of the rat reticulocyte energy metabolism and hormonal responsiveness[J]. Biomed Biochim Acta, 1990, 49(2-3):S178-S182.
[8] Harris JJ, Attwell D. The energetics of CNS white matter[J]. J Neurosci, 2012, 32(1):356-371.
[9] Bizzozero OA, Sanchez P, Tetzloff SU. Effect of ATP depletion on the palmitoylation of myelin proteolipid protein in young and adult rats[J]. J Neurochem, 1999, 72(6):2610-2616.
[10] Rinholm JE, Vervaeke K, Tadross MR, et al. Movement and structure of mitochondria in oligodendrocytes and their myelin sheaths[J]. Glia, 2016, 64(5):810-825.
[11] Leoni V, Caccia C. The impairment of cholesterol metabolism in Huntington disease[J]. Biochim Biophys Acta, 2015, 1851(8):1095-1105.
[12] Voccoli V, Tonazzini I, Signore G, et al. Role of extracellular calcium and mitochondrial oxygen species in psychosineinduced oligodendrocyte cell death[J]. Cell Death Dis, 2014, 5:e1529.
[13] Yagi M, Uchiumi T, Sagata N, et al. Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration[J]. Sci Rep, 2017, 7(1):15131.
[14] Area-Gomez E, de Groof A, Bonilla E, et al. A key role for MAM in mediating mitochondrial dysfunction in Alzheimer disease[J]. Cell Death Dis, 2018, 9(3):335.
[15] Bannwarth S, Ait-El-Mkadem S, Chaussenot A, et al. A mitochondrial origin for frontotemporal dementia and amyotrophic lateral sclerosis through CHCHD10 involvement[J]. Brain, 2014, 137(Pt 8):2329-2345.
[16] Toldo I, Nosadini M, Boscardin C, et al. Neonatal mitochondrial leukoencephalopathy with brain and spinal involvement and high lactate:expanding the phenotype of ISCA2 gene mutations[J]. Metab Brain Dis, 2018, 33(3):805-812.
[17] Vanopdenbosch L, Dubois B, D'Hooghe MB, et al. Mitochondrial mutations of Leber's hereditary optic neuropathy:a risk factor for multiple sclerosis[J]. J Neurol, 2000, 247(7):535-543.
[18] Rezaee AR, Azadi A, Houshmand M, et al. Mitochondrial and nuclear genes as the cause of complex I deficiency[J]. Genet Mol Res, 2013, 12(3):3551-3554.
[19] Yagi M, Uchiumi T, Sagata N, et al. Neural-specific deletion of mitochondrial p32/C1qbp leads to leukoencephalopathy due to undifferentiated oligodendrocyte and axon degeneration[J]. Sci Rep, 2017, 7(1):15131.
[20] Graham EM, Burd I, Everett AD, et al. Blood biomarkers for evaluation of perinatal encephalopathy[J]. Front Pharmacol, 2016, 7:196.
[21] Inder T, Mocatta T, Darlow B, et al. Elevated free radical products in the cerebrospinal fluid of VLBW infants with cerebral white matter injury[J]. Pediatr Res, 2002, 52(2):213-218.
[22] González-Fernández E, Sánchez-Gómez MV, Pérez-Samartín A, et al. A3 Adenosine receptors mediate oligodendrocyte death and ischemic damage to optic nerve[J]. Glia, 2014, 62(2):199-216.
[23] Kim JY, Lee EY, Sohn HJ, et al. Differential expression of αB-crystallin causes maturation-dependent susceptibility of oligodendrocytes to oxidative stress[J]. BMB Rep, 2013, 46(10):501-506.
[24] Miyamoto N, Maki T, Pham LD, et al. Oxidative stress interferes with white matter renewal after prolonged cerebral hypoperfusion in mice[J]. Stroke, 2013, 44(12):3516-3521.
[25] Takase H, Liang AC, Miyamoto N, et al. Protective effects of a radical scavenger edaravone on oligodendrocyte precursor cells against oxidative stress[J]. Neurosci Lett, 2018, 668:120-125.
[26] O'Hare Doig RL, Bartlett CA, Maghzal GJ, et al. Reactive species and oxidative stress in optic nerve vulnerable to secondary degeneration[J]. Exp Neurol, 2014, 261:136-146.
[27] Mendivil-Perez M, Soto-Mercado V, Guerra-Librero A, et al. Melatonin enhances neural stem cell differentiation and engraftment by increasing mitochondrial function[J]. J Pineal Res, 2017, 63:e12415.
[28] Nuñez A, Benavente I, Blanco D, et al. Oxidative stress in perinatal asphyxia and hypoxic-ischaemic encephalopathy[J]. An Pediatr (Barc), 2018, 88(4):228.e1-228.e9.
[29] Lee GH, Lee HY, Li B, et al. Bax Inhibitor-1-mediated inhibition of mitochondrial Ca2+ intake regulates mitochondrial permeability transition pore opening and cell death[J]. Sci Rep, 2014, 4:5194.
[30] Milbourn HR, Toomey LM, Gavriel N, et al. Limiting oxidative stress following neurotrauma with a combination of ion channel inhibitors[J]. Discov Med, 2017, 23(129):361-369.
[31] Schoenfeld R, Wong A, Silva J, et al. Oligodendroglial differentiation induces mitochondrial genes and inhibition of mitochondrial function represses oligodendroglial differentiation[J]. Mitochondrion, 2010, 10(2):143-150.
[32] Wang Y, Zhang Y, He J, et al. Hyperforin promotes mitochondrial function and development of oligodendrocytes[J]. J Neurochem, 2011, 119(3):555-568.
[33] Heidker RM, Emerson MR, Levine SM. Metabolic pathways as possible therapeutic targets for progressive multiple sclerosis[J]. Neural Regen Res, 2017, 12(8):1262-1267.
[34] Singhal NK, Alkhayer K, Shelestak J, et al. Erythropoietin upregulates brain hemoglobin expression and supports neuronal mitochondrial activity[J]. Mol Neurobiol, 2018, 55(10):8051-8058.
[35] Juliano C, Sosunov S, Niatsetskaya Z, et al. Mild intermittent hypoxemia in neonatal mice causes permanent neurofunctional deficit and white matter hypomyelination[J]. Exp Neurol, 2015, 264:33-42.
[36] Douglas RM, Ryu J, Kanaan A, et al. Neuronal death during combined intermittent hypoxia/hypercapnia is due to mitochondrial dysfunction[J]. Am J Physiol Cell Physiol, 2010, 298(6):C1594-C1602.
[37] Rone MB, Cui QL, Fang J, et al. Oligodendrogliopathy in multiple sclerosis:low glycolytic metabolic rate promotes oligodendrocyte survival[J]. J Neurosci, 2016, 36(17):4698-4707.
[38] Su X, Yuan H, Cui H, et al. Effect of T helper cell 1/T helper cell 2 balance and nuclear factor-κB on white matter injury in premature neonates[J]. Mol Med Rep, 2018, 17(4):5552-5556.
[39] Elovitz MA, Mrinalini C, Sammel MD. Elucidating the early signal transduction pathways leading to fetal brain injury in preterm birth[J]. Pediatr Res, 2006, 59(1):50-55.
[40] Bonora M, De Marchi E, Patergnani S, et al. Tumor necrosis factor-α impairs oligodendroglial differentiation through a mitochondria-dependent process[J]. Cell Death Differ, 2014, 21(8):1198-1208.
[41] Chamberlain KA, Chapey KS, Nanescu SE, et al. Creatine enhances mitochondrial-mediated oligodendrocyte survival after demyelinating injury[J]. J Neurosci, 2017, 37(6):1479-1492.
[42] 李明熹, 母得志. 线粒体自噬与神经系统疾病[J]. 中国当代儿科杂志, 2017, 19(6):724-728.
[43] Cavallucci V, Bisicchia E, Cencioni MT, et al. Acute focal brain damage alters mitochondrial dynamics and autophagy in axotomized neurons[J]. Cell Death Dis, 2014, 5:e1545.
[44] Kim H, Lee JY, Park KJ, et al. A mitochondrial division inhibitor, Mdivi-1, inhibits mitochondrial fragmentation and attenuates kainic acid-induced hippocampal cell death[J]. BMC Neurosci, 2016, 17(1):33.
[45] Yu S, Zheng S, Leng J, et al. Inhibition of mitochondrial calcium uniporter protects neurocytes from ischemia/reperfusion injury via the inhibition of excessive mitophagy[J]. Neurosci Lett, 2016, 628:24-29.