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Abstract
Exenatide is associated with increased OPA1 expression and enhanced Drp1 phosphorylation at Ser637 after spinal cord injury.
- Mitochondrial dysfunction is a significant factor in the progression of neuronal damage following spinal cord injury.
- Exenatide treatment may promote a shift toward mitochondrial fusion by increasing specific protein expressions.
- The expression of Bcl-2, HO-1, and p62 tended to increase with exenatide treatment.
- In cell cultures, exenatide reduced the negative effects of oxidative stress on cell viability and preserved mitochondrial function.
- These findings suggest that exenatide may help reduce secondary injury after spinal cord injury by supporting mitochondrial health.
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