AI Article Synopsis
- Spinal cord injury (SCI) causes neurological dysfunction primarily due to neuronal cell death, which includes various types of programmed cell death (PCD) beyond just necrosis and apoptosis.
- Recent research has identified additional forms of PCD, such as pyroptosis, necroptosis, ferroptosis, and cuproptosis, all of which play significant roles in the progression of SCI.
- Understanding these mechanisms opens up potential therapeutic avenues to regulate neuronal cell death and improve recovery of neural function after SCI.
Article Abstract
Spinal cord injury (SCI) often leads to neurological dysfunction, and neuronal cell death is one of the main causes of neurological dysfunction. After SCI, in addition to necrosis, programmed cell death (PCD) occurs in nerve cells. At first, studies recognized only necrosis, apoptosis, and autophagy. In recent years, researchers have identified new forms of PCD, including pyroptosis, necroptosis, ferroptosis, and cuproptosis. Related studies have confirmed that all of these cell death modes are involved in various phases of SCI and affect the direction of the disease through different mechanisms and pathways. Furthermore, regulating neuronal cell death after SCI through various means has been proven to be beneficial for the recovery of neural function. In recent years, emerging therapies for SCI have also provided new potential methods to restore neural function. Thus, the relationship between SCI and cell death plays an important role in the occurrence and development of SCI. This review summarizes and generalizes the relevant research results on neuronal necrosis, apoptosis, autophagy, pyroptosis, necroptosis, ferroptosis, and cuproptosis after SCI to provide a new understanding of neuronal cell death after SCI and to aid in the treatment of SCI.
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| http://dx.doi.org/10.1007/s12035-024-04188-3 | DOI Listing |
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