Metabolomics-driven exploration of sphingosine 1-phosphate mechanisms in refractory epilepsy

This study aims to investigate the role of sphingosine 1-phosphate (S1P) in refractory epilepsy (RE) and elucidate its underlying molecular mechanisms. We employed metabolomics technology to analyze serum metabolites and gene expression patterns in individuals with RE. Additional omics analyses were conducted using cellular and animal models to explore the specific functions of S1P and related metabolic pathways. Our findings demonstrated that ACER3/SphK1/S1P play protective roles in maintaining mitochondrial structure and function. These elements were shown to mitigate neuronal hyperexcitability and protect against neuronal damage. By elucidating the dysregulation of metabolic pathways associated with disease onset and progression, our research illuminated the impact of abnormal sphingolipid metabolism and gene expression variances on the manifestation and progression of RE. This research underscores the critical impact of abnormal sphingolipid metabolism on RE development and progression. The insights gained from this study provide a foundation for developing targeted pharmaceutical interventions and symptomatic treatments for individuals with RE.

Cognitive function; Electroencephalogram; Metabolomics; Mitochondrial abnormality; Refractory epilepsy; Sphingolipid metabolism; Sphingosine 1-phosphate.