The mechanism of the JNK signaling pathway in drug addiction : Author list.

Abstract

Drug addiction is a multifactorial neurofunctional disorder influenced by a complex interplay of environmental, biological, and genetic factors. Recent studies have demonstrated that aberrant activation of the c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in the development of drug addiction. JNK, a member of the mitogen-activated protein kinase (MAPK) family, participates in neural development during embryogenesis and regulates neuronal proliferation and differentiation in adulthood, thereby maintaining the functional integrity of neural stem and progenitor cells and preserving appropriate brain plasticity and homeostasis. By modulating key biological processes such as inflammation, oxidative stress, autophagy, and apoptosis, the JNK signaling pathway regulates neuronal homeostasis and synaptic plasticity and contributes to the molecular mechanisms underlying drug addiction. In addition, JNK signaling influences addiction-related epigenetic regulation by modulating DNA methylation. This review comprehensively analyzes the involvement of the JNK signaling pathway in drug addiction, to broaden current perspectives on addiction research and inform the development of novel therapeutic strategies.