Abstract
The c-Jun N-terminal kinase (JNK) signalling pathway is a conserved response to a wide range of internal and external cellular stress signals. Beside the stress response, the JNK pathway is involved in a series of vital regulatory mechanisms during development and adulthood that are critical to maintain tissue homeostasis. These mechanisms include the regulation of apoptosis, growth, proliferation, differentiation, migration and invasion. The JNK pathway has a diverse functionality and cell-tissue specificity, and has emerged as a key player in regeneration, tumorigenesis and other pathologies. The JNK pathway is highly active in the central nervous system (CNS), and plays a central role when cells need to cope with pathophysiological insults during development and adulthood. Here, we review the implications of the JNK pathway in pathologies of the CNS. More specifically, we discuss some newly identified examples and mechanisms of JNK-driven tumor progression in glioblastoma, regeneration/repair after an injury, neurodegeneration and neuronal cell death. All these new discoveries support the central role of JNK in CNS pathologies and reinforce the idea of JNK as potential target to reduce their detrimental effects.
Highlights
The central nervous system (CNS) is exposed to stress stimuli during development and adulthood, and under pathological aggressions
The Jun N-terminal kinase signalling pathway (JNK) pathway includes a conserved mitogen-activated protein kinase (MAPK), which belongs to the stress-activated protein kinase (SAPK) group, a group of kinases that can be activated by any internal or external stimuli that cause cell stress
These results indicate that JNK signalling plays a central role in Alzheimer’s Disease (AD) neurodegeneration, but JNK has emerged as a potential biomarker for early diagnosis, and a potential target to prevent neuronal cell death [55]
Summary
The CNS is exposed to stress stimuli during development and adulthood, and under pathological aggressions These events trigger the Jun N-terminal kinase signalling pathway (JNK) as a mechanism to coordinate cellular responses to stress, and maintain tissue homeostasis. AP1/dAP-1 modulates the transcriptional program ofFos/Jay, genes involved variety of biological activities.AP1/dAP-1 This pathway can be activated at other steps indicated with dotted in lines in the of diagram. Sci. 2021, 22, 3883 pathway in cell death and cell survival, depending on the cell type and the context [11] This two-faded role is important in CNS pathologies such as neurodegeneration and tumorigenesis, in which the cellular stress-associated signals are increased [29,30]. We describe how neurons and glia regulate stressful environments such as brain tumors, acute injuries or neurodegenerative diseases through the JNK pathway
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