The c-Jun N-terminal kinase signaling pathway in epilepsy: activation, regulation, and therapeutics

Abstract

Epilepsy affects approximately 50–70 million people worldwide and 30–40% of patients do not benefit from medication. Therefore, it is necessary to identify novel targets for epileptic treatments. c-Jun N-terminal kinase (JNK) is a member of the mitogen-activated protein kinase (MAPK) family that activates diverse substrates, such as transcriptional factors, adaptor proteins, and signaling proteins, and has a wide variety of functions in both physiological and pathological conditions. The excessive activation of JNK is found not only in the acute phase of epilepsy, but also in the chronic phase, which potentiates it as a promising target in epilepsy control. In this review, we discuss the activation of the JNK pathway in epilepsy and its role in neuronal death, astrocyte activation, and mossy fiber sprouting (MFS) based on recent updates. Finally, we briefly introduce the current agents that target JNK signaling to control epilepsy.

Keywords:

• c-Jun NH2-terminal kinase pathway
• epilepsy
• neuronal death
• mossy fiber sprouting
• astrocyte activation

Disclosure statement

No potential conflict of interest was reported by the authors.