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Vol 56(2022) N 6 p. 967-978; DOI 10.1134/S0026893322060115 Full Text

M.S. Kukharsky1,2*, M.W. Everett1, O.A. Lytkina2, M.A. Raspopova2, E.A. Kovrazhkina3, R.K. Ovchinnikov1,2, A.I. Antohin1, A.A. Moskovtsev1,4

Protein Homeostasis Dysregulation in Pathogenesis of Neurodegenerative Diseases

1Pirogov Russian National Research Medical University, Ministry of Health of the Russian Federation, Moscow, 117997 Russia
2Institute of Physiologically Active Compounds, Russian Academy of Sciences, Chernogolovka, Moscow oblast, 142432 Russia
3Federal Centre for Brain and Neurotechnologies, Federal Medical and Biological Agency, Moscow, 117997 Russia
4Institute of General Pathology and Pathophysiology, Moscow, 125315 Russia

*kukharskym@gmail.com
Received - 2022-05-05; Revised - 2022-05-05; Accepted - 2022-05-31

The formation and accumulation of unfolded, misfolded, or damaged cellular proteins leads to development of endoplasmic reticulum stress (ER stress). A series of protective reactions is initiated in response to ER stress. These reactions are aimed at restoring the balance between protein synthesis and degradation, which is key to maintaining protein homeostasis (proteostasis). The main protective mechanisms are the attenuation of protein synthesis, increase of chaperone levels, and activation of protein degradation systems. Insufficiency or malfunction of these mechanisms induce apoptosis. Proteostasis dysregulation accompanied by protein aggregation and subsequent cell death in specific regions of the nervous system is a common pathogenetic hallmark of most neurodegenerative diseases. We discuss targeted regulation of the ER stress signaling pathways as a potential therapeutic strategy that can slow or even halt the disease progression.

ER stress, protein aggregation, proteostasis, neurodegenerative diseases



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