Abstract: 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 barrier, vascular injury, glial reactivity, neuroinflammation, 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).