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作 者:Seyed Mojtaba Hosseini Soheila Karimi-Abdolrezaee
机构地区:[1]Department of Physiology and Pathophysiology,Spinal Cord Research Centre,Rady Faculty of Health Sciences,University of Manitoba,Winnipeg,MB,Canada [2]Manitoba Multiple Sclerosis Research Center,Winnipeg,MB,Canada [3]Children Hospital Research Institute of Manitoba,Winnipeg,MB,Canada
出 处:《Neural Regeneration Research》2025年第6期1699-1700,共2页中国神经再生研究(英文版)
基 金:funding support from the Canadian Institutes of Health Research;supported by a Doctoral Studentship from the Wings for Life Foundation。
摘 要:Extensive neurodegeneration is a hallmark of traumatic spinal cord injury (SCI) that underlies permanent sensorimotor and autonomic impairments (Alizadeh et al.,2019).Following the primary impact,the spinal cord undergoes a cascade of secondary injury mechanisms that are driven by disruption of the blood-spinal cord ba rrier,vascula r inju ry,glial reactivity,neu roinfla mmation,oxidative stress,lipid peroxidation,and glutamate excitotoxicity that culminate in neuronal and oligodendroglial cell death,demyelination,and axonal damage(Alizadeh et al.,2019).To achieve a meaningful functional recovery after SCI,regeneration of new neurons and oligodendrocytes and their successful growth and integration within the neural network are critical steps for reconstructing the damaged spinal cord tissue (Fischer et al.,2020).
关 键 词:PEROXIDATION FISCHER INJURY
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