The role of endoplasmic reticulum stress in astrocytes.

Autor: Sims SG; Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia, USA., Cisney RN; Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia, USA., Lipscomb MM; Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia, USA., Meares GP; Department of Microbiology, Immunology, and Cell Biology, West Virginia University, Morgantown, West Virginia, USA.; Department of Neuroscience, West Virginia University, Morgantown, West Virginia, USA.; Rockefeller Neuroscience Institute, Morgantown, West Virginia, USA.
Jazyk: angličtina
Zdroj: Glia [Glia] 2022 Jan; Vol. 70 (1), pp. 5-19. Date of Electronic Publication: 2021 Aug 31.
DOI: 10.1002/glia.24082
Abstrakt: Astrocytes are glial cells that support neurological function in the central nervous system (CNS), in part, by providing structural support for neuronal synapses and blood vessels, participating in electrical and chemical transmission, and providing trophic support via soluble factors. Dysregulation of astrocyte function contributes to neurological decline in CNS diseases. Neurological diseases are highly heterogeneous but share common features of cellular stress including the accumulation of misfolded proteins. Endoplasmic reticulum (ER) stress has been reported in nearly all neurological and neurodegenerative diseases. ER stress occurs when there is an accumulation of misfolded proteins in the ER lumen and the protein folding demand of the ER is overwhelmed. ER stress initiates the unfolded protein response (UPR) to restore homeostasis by abating protein translation and, if the cell is irreparably damaged, initiating apoptosis. Although protein aggregation and misfolding in neurological disease has been well described, cell-specific contributions of ER stress and the UPR in physiological and disease states are poorly understood. Recent work has revealed a role for active UPR signaling that may drive astrocytes toward a maladaptive phenotype in various model systems. In response to ER stress, astrocytes produce inflammatory mediators, have reduced trophic support, and can transmit ER stress to other cells. This review will discuss the current known contributions and consequences of activated UPR signaling in astrocytes.
(© 2021 The Authors. GLIA published by Wiley Periodicals LLC.)
Databáze: MEDLINE
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