FIGURE 1.

The relationship of redox-related cell death and epilepsy. Under the exposure of toxins, such as high levels of Glu, NMDA, and KA as well as low GABA content, neuronal hyperexcitation occurs, leading to ROS accumulation. Oxidative stress induced by redox unbalance then leads to multiple types of redox-associated neuronal death modes including apoptosis, autophagy, necroptosis, pyroptosis, and ferroptosis by activating caspase-3, LC3II expression, MLKL phosphorylation, caspase-1 activation and Gpx4 activity, respectively. Within a cell, the molecular crosstalk of these cell death modalities occurs, which ultimately triggers dead neuron phenotype and provokes epilepsy. Meanwhile, the recurrent epileptic seizures also have the capacity of exacerbating neuronal excitotoxicity and overproduction of ROS, shaping a vicious circle.