Spinal cord injury (SCI) is one of the leading causes of long-term disability and death worldwide. In the United States alone, SCI has an annual incidence of 12,000-20,000 cases, affecting a total of nearly half a million patients. Clinically, the treatments of SCI mainly include methylprednisolone, surgical decompression, supportive medical care, and rehabilitation. However, patient recovery is limited. Thus, new ideas and therapeutic targets are needed for the development of new and effective SCI treatments.

During SCI, neuronal cell death is an important pathological event contributing to neurological deficits. Mechanistically, the majority of neuronal cell death is not due to direct mechanical damage, but rather to damage-induced biochemical disruptions, such as oxidative stress, as part of secondary injury. Excessive reactive oxygen species (ROS) induces cell death (such as autophagy, pyroptosis, and necroptosis) in neurons and oligodendrocytes, which significantly limits neural regeneration and repair after SCI. Despite playing a clear pathological role in SCI, the mechanism and signalling pathways of oxidative stress during secondary injury remains unknown.

The aim of this Special Issue, therefore, is to investigate the critical role that oxidative stress plays in regulating cell death and nerve regeneration in SCI, and to explore its potential as a promising therapeutic target for future treatments of SCI. Papers investigating the molecular mechanisms of oxidative stress in SCI and the interaction between oxidative stress and autophagy in SCI are especially welcome. We welcome both original research and review articles.

Potential topics include but are not limited to the following:

• Sources of reactive oxygen species in spinal cord injury
• Molecular mechanisms of oxidative stress in spinal cord injury
• The role of oxidative stress in cell death and nerve regeneration after spinal cord injury
• The interaction of oxidative stress and autophagy in the pathophysiology of spinal cord injury