Proteostasis During Cerebral Ischemia

Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles...

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Vydané v:Frontiers in neuroscience Ročník 13; s. 637
Hlavní autori: Thiebaut, Audrey M., Hedou, Elodie, Marciniak, Stefan J., Vivien, Denis, Roussel, Benoit D.
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Switzerland Frontiers Research Foundation 19.06.2019
Frontiers Media S.A
Predmet:
Apoptosis
Autophagy
Brain research
Cell death
Cell survival
Diabetes
Endoplasmic reticulum
ER stress
Homeostasis
Hypoxia
Ischemia
Kinases
mTOR
Neurological disorders
Neuroscience
Phagocytosis
Protein biosynthesis
Protein folding
Protein synthesis
Protein transport
Proteins
proteostasis
Stroke
United Kingdom > UK
France
ER stress
mTOR
autophagy
proteostasis
stroke
ISSN:1662-453X, 1662-4548, 1662-453X
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Abstract Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in the regulation of proteostasis: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however, their over-activation in duration or intensity can lead to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. A better understanding of autophagy and ER stress will allow the development of therapeutic strategies for stroke, both at the acute phase and during recovery. This review summarizes the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. We argue that the processes governing proteostasis should be considered together in stroke, rather than focusing either on ER stress or autophagy in isolation.
AbstractList Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding and transport; and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in proteostasis’ regulation: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however their overactivation in time or intensity often leads to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. Better comprehension of autophagy and ER stress will allow therapeutic strategies for stroke both at the acute phase and during recovery. The interest of this review is to summarize the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. In addition, we discuss the interest to study proteostasis as a single pathway rather than studying either ER stress or autophagy in stroke.
Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in the regulation of proteostasis: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however, their over-activation in duration or intensity can lead to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. A better understanding of autophagy and ER stress will allow the development of therapeutic strategies for stroke, both at the acute phase and during recovery. This review summarizes the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. We argue that the processes governing proteostasis should be considered together in stroke, rather than focusing either on ER stress or autophagy in isolation.
Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in the regulation of proteostasis: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however, their over-activation in duration or intensity can lead to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. A better understanding of autophagy and ER stress will allow the development of therapeutic strategies for stroke, both at the acute phase and during recovery. This review summarizes the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. We argue that the processes governing proteostasis should be considered together in stroke, rather than focusing either on ER stress or autophagy in isolation.Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis refers to the equilibrium between protein synthesis, folding, transport, and protein degradation. Within the brain proteostasis plays key roles in learning and memory by controlling protein synthesis and degradation. Two important pathways are implicated in the regulation of proteostasis: the unfolded protein response (UPR) and macroautophagy (called hereafter autophagy). Both are necessary for cell survival, however, their over-activation in duration or intensity can lead to cell death. Moreover, UPR and autophagy can activate and potentiate each other to worsen the issue of cerebral ischemia. A better understanding of autophagy and ER stress will allow the development of therapeutic strategies for stroke, both at the acute phase and during recovery. This review summarizes the latest therapeutic advances implicating ER stress or autophagy in cerebral ischemia. We argue that the processes governing proteostasis should be considered together in stroke, rather than focusing either on ER stress or autophagy in isolation.
Author Vivien, Denis
Thiebaut, Audrey M.
Hedou, Elodie
Roussel, Benoit D.
Marciniak, Stefan J.
AuthorAffiliation 2 Cambridge Institute for Medical Research, University of Cambridge , Cambridge , United Kingdom
4 Department of Clinical Research, University of Caen Normandy , Caen , France
1 INSERM, INSERM UMR-S U1237, Physiopathology and Imaging of Neurological Disorders, University of Caen Normandy , Caen , France
3 Department of Medicine, Addenbrooke’s Hospital, University of Cambridge , Cambridge , United Kingdom
AuthorAffiliation_xml – name: 4 Department of Clinical Research, University of Caen Normandy , Caen , France
– name: 2 Cambridge Institute for Medical Research, University of Cambridge , Cambridge , United Kingdom
– name: 3 Department of Medicine, Addenbrooke’s Hospital, University of Cambridge , Cambridge , United Kingdom
– name: 1 INSERM, INSERM UMR-S U1237, Physiopathology and Imaging of Neurological Disorders, University of Caen Normandy , Caen , France
Author_xml – sequence: 1
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  surname: Thiebaut
  fullname: Thiebaut, Audrey M.
– sequence: 2
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  surname: Vivien
  fullname: Vivien, Denis
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  givenname: Benoit D.
  surname: Roussel
  fullname: Roussel, Benoit D.
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Copyright © 2019 Thiebaut, Hedou, Marciniak, Vivien and Roussel. 2019 Thiebaut, Hedou, Marciniak, Vivien and Roussel
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Keywords ER stress
mTOR
autophagy
proteostasis
stroke
Language English
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Edited by: Mathias Gelderblom, University Medical Center Hamburg-Eppendorf, Germany
This article was submitted to Neurodegeneration, a section of the journal Frontiers in Neuroscience
These authors have contributed equally to this work
Reviewed by: Pedro Domingos, Institute of Chemical and Biological Technology, New University of Lisbon, Portugal; Maria Xilouri, Biomedical Research Foundation of the Academy of Athens, Greece
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Snippet Cerebral ischemia is a complex pathology involving a cascade of cellular mechanisms, which deregulate proteostasis and lead to neuronal death. Proteostasis...
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SubjectTerms Apoptosis
Autophagy
Brain research
Cell death
Cell survival
Diabetes
Endoplasmic reticulum
ER stress
Homeostasis
Hypoxia
Ischemia
Kinases
mTOR
Neurological disorders
Neuroscience
Phagocytosis
Protein biosynthesis
Protein folding
Protein synthesis
Protein transport
Proteins
proteostasis
Stroke
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