Central nervous system (CNS) trauma, including traumatic brain injury (TBI) and spinal cord injury (SCI) is one of the leading causes of long-term disability and death worldwide. Clinically, the treatments of CNS trauma 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 CNS trauma treatments.
During CNS trauma, neuronal programmed cell death is an important pathological event contributing to neurological deficits. Mechanistically, the majority of neuronal programmed cell death is not due to direct mechanical damage, but rather to damage-induced biochemical disruptions such as oxidative stress and inflammation as parts of secondary injury. It was realized that programmed cell death (such as autophagy, pyroptosis and necroptosis ) occurs in neurons, microglia, and oligodendrocytes, which significantly limits neural regeneration and repair after CNS trauma treatments. Despite playing a clear pathological role in CNS trauma, the mechanism and signaling pathways of programmed cell death during secondary injury remains unknown.
It is believed that in CNS trauma treatments, programmed cell death plays a critical role in regulating nerve regeneration, and may be a promising therapeutic target for the future treatments of CNS trauma.
This Research Topic therefore aims to investigate the following areas:
1. Molecular mechanisms of programmed cell death in CNS trauma;
2. The role of programmed cell death in nerve regeneration after CNS trauma;
3. The interaction of programmed cell death and neural repair in the pathophysiology of CNS trauma treatments.
Central nervous system (CNS) trauma, including traumatic brain injury (TBI) and spinal cord injury (SCI) is one of the leading causes of long-term disability and death worldwide. Clinically, the treatments of CNS trauma 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 CNS trauma treatments.
During CNS trauma, neuronal programmed cell death is an important pathological event contributing to neurological deficits. Mechanistically, the majority of neuronal programmed cell death is not due to direct mechanical damage, but rather to damage-induced biochemical disruptions such as oxidative stress and inflammation as parts of secondary injury. It was realized that programmed cell death (such as autophagy, pyroptosis and necroptosis ) occurs in neurons, microglia, and oligodendrocytes, which significantly limits neural regeneration and repair after CNS trauma treatments. Despite playing a clear pathological role in CNS trauma, the mechanism and signaling pathways of programmed cell death during secondary injury remains unknown.
It is believed that in CNS trauma treatments, programmed cell death plays a critical role in regulating nerve regeneration, and may be a promising therapeutic target for the future treatments of CNS trauma.
This Research Topic therefore aims to investigate the following areas:
1. Molecular mechanisms of programmed cell death in CNS trauma;
2. The role of programmed cell death in nerve regeneration after CNS trauma;
3. The interaction of programmed cell death and neural repair in the pathophysiology of CNS trauma treatments.
