Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

JNK Pathway in CNS Pathologies

Version 1 : Received: 21 February 2021 / Approved: 23 February 2021 / Online: 23 February 2021 (08:15:48 CET)

A peer-reviewed article of this Preprint also exists.

de los Reyes Corrales, T.; Losada-Pérez, M.; Casas-Tintó, S. JNK Pathway in CNS Pathologies. Int. J. Mol. Sci. 2021, 22, 3883. de los Reyes Corrales, T.; Losada-Pérez, M.; Casas-Tintó, S. JNK Pathway in CNS Pathologies. Int. J. Mol. Sci. 2021, 22, 3883.

Journal reference: Int. J. Mol. Sci. 2021, 22, 3883
DOI: 10.3390/ijms22083883

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. Besides 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 such a diverse functionality and cell-tissue specificity, that it has emerged as a key player in regeneration, tumorigenesis and other pathologies such as neurodegenerative diseases. The JNK pathway is highly active in the central nervous system (CNS), and plays a central role for the cells to cope with pathophysiological insults during both development and adulthood. Among the many mechanisms described in the literature, in this review we focus on the JNK pathway functions 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 in the CNS, neurodegeneration, and neuronal cell death. Recent studies have shown that the JNK pathway regulates matrix metalloproteinases (MMPs) production in response to cytoneme/tumor microtubes formation and Wingless (Wg)/WNT pathway activation in glioblastoma cells. Thus, JNK pathway is essential for glioblastoma progression, infiltration and non-autonomous induction of neurodegeneration. In regeneration, the JNK pathway controls Draper (Drpr) expression in glial cells that mediate engulfment and regeneration of the CNS upon injury.

Subject Areas

Glioblastoma; Neurodegeneration; Injury; Regeneration; Drosophila

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