This research shows S1P1 regulates neuronal injury in epilepsy, suggesting targeting S1P1 may reduce inflammation and oxidative stress effects.
S1P1-PHB2 axis plays a crucial role in the neuroinflammation and neurodamage caused by epilepsy. S1P1, through PHB2, promotes mitochondrial autophagy, increases oxidative stress and releases pro-inflammatory cytokines, thereby leading to neural damage. By using the S1P1 antagonist W146 to inhibit autophagy and inflammatory responses, these effects can be alleviated.
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Yang et al. (2025) studied this question.
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