Alterations of JNK Signaling Pathway Activity in the Rat Retina: Effects of Age, Age-Related Macular Degeneration-like Pathology, and a JNK Inhibitor (IQ-1S)

Bibliographic Details
Parent link:Cells.— .— Basel: MDPI AG
Vol. 14, iss. 12.— 2025.— Article number 896, 17 p.
Other Authors: Muraleva Natalia, Tikhonov D. I. Dmitry, Zhdankina A. A. Anna, Plotnikov M. B. Mark, Khlebnikov A. I. Andrey Ivanovich, Logvinov S. V. Sergey Valentinovich, Kolosova N. G. Nataliya
Summary:Age-related macular degeneration (AMD) is the leading cause of irreversible visual impairment worldwide. AMD development is associated with inflammation, oxidative stress, and a progressive proteostasis imbalance, in whose regulation, c-Jun N-terminal kinases (JNKs) play a crucial role. JNK inhibition is being discussed as a new way to prevent and treat AMD, but there are no data on JNK signaling in the retina and its changes with age and with AMD development. Here, for the first time, we assessed JNK-signaling activity in the retina and did not detect its age-related changes in healthy Wistar rats. By contrast, manifestation and progression of the AMD-like pathology in OXYS rats occurred simultaneously with JNK pathway activation. We also confirmed that selective JNK3 inhibitor 11H-indeno[1,2-b]quinoxalin-11-one oxime sodium salt (IQ-1S) can suppress neurodegenerative changes in the OXYS rat retina. Its effects were prevention of the destructive changes in retinal synapses and the suppression of the JNK signaling pathway activity during active progression of AMD signs in OXYS rats
Текстовый файл
Published: 2025
Subjects:
Online Access:https://doi.org/10.3390/cells14120896
Format: Electronic Book Chapter
KOHA link:https://koha.lib.tpu.ru/cgi-bin/koha/opac-detail.pl?biblionumber=682259