Editorial: Restoring neural circuits after spinal cord injury

Spinal cord injury (SCI) leads to dysfunction in the spinal cord at and below the site of injury, resulting in impairments such as paralysis of movement and sensation. During SCI, the primary injury triggers the production of free radicals, leading to a chronic state of ischemia and hypoxia. This results in glutamate excitotoxicity, lipid peroxidation, calcium influx, edema, and cellular damage. Neural circuits exist in the spinal cord throughout an individual’s life and are crucial for recovering locomotor function below the level of injury.

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  iPSCs have the potential to differentiate into neurons, astrocytes, and oligodendrocytes, replacing damaged cells, regulating the spinal cord microenvironment, and promoting axon and myelin sheath regeneration.
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  MicroRNAs have emerged as critical regulators in the molecular landscape of neural repair, especially following SCI, by modulating inflammatory responses, promoting neuronal survival, enhancing axonal regrowth, and facilitating myelin repair.
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  Resting-state functional magnetic resonance imaging (rsfMRI) revealed that the primary and secondary motor cortex holds high centrality post-injury, signifying their importance in motor function.