UCP2 and status epilepticus: In animal studies, several endogenous protective mechanisms to reduce seizure-induced neuronal damage following status epilepticus have been proposed, including epileptic tolerance, enhanced vascular endothelial growth factors, activation of the ERK1/2 pathway, and activation of the adenosine A1 receptors, erythropoietin receptor, and mitochondrial uncoupling protein 2 (UCP2) [27,51,52,53,54,55].