Application and prospects of somatic cell reprogramming technology for spinal cord injury treatment.

Spinal cord injury (SCI) is a serious neurological trauma that is challenging to treat. After SCI, many neurons in the injured area die due to necrosis or apoptosis, and astrocytes, oligodendrocytes, microglia and other non-neuronal cells become dysfunctional, hindering the repair of the injured spinal cord. Corrective surgery and biological, physical and pharmacological therapies are commonly used treatment modalities for SCI; however, no current therapeutic strategies can achieve complete recovery.

Knockdown of polypyrimidine tract binding protein facilitates motor function recovery after spinal cord injury.

After spinal cord injury (SCI), a fibroblast- and microglia-mediated fibrotic scar is formed in the lesion core, and a glial scar is formed around the fibrotic scar as a result of the activation and proliferation of astrocytes. Simultaneously, a large number of neurons are lost in the injured area. Regulating the dense glial scar and replenishing neurons in the injured area are essential for SCI repair.

Downregulation of Nck1 After Spinal Cord Injury in Adult Rats.

Background: Nck1 is an important molecule that participates in many cellular processes, including neurite outgrowth, synaptic plasticity, and apoptosis. However, the expression and function of Nck1 in the spinal cord and spinal cord injury remain unknown.

Aims: To investigate the role of Nck1 in spinal cord injury.