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doi: 10.1017/erm.2017.9 86 GleasonA.BushA

Epileptogenic injuries or seizures initiate the synthesis and secretion of proinflammatory molecules such as TNF-, IL-1, and High Mobility Group Box 1 (HMGB1) in glial cells which result in decreasing seizure threshold, which further contributes to seizure precipitation, and recurrence because of rapid changes in glutamate and -aminobutyric acid (GABA) receptor phosphorylation

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FADS2-dependent fatty acid desaturation dictates cellular sensitivity to ferroptosis and permissiveness for hepatitis C virus replication