How cytosolic compartments play safeguard functions against neuroinflammation and cell death in cerebral ischemia

Ischemic stroke is the second leading cause of mortality and disability globally. Neuronal damage following ischemic stroke is rapid and irreversible, and eventually results in neuronal death. In addition to activation of cell death signaling, neuroinflammation is also considered as another pathogen...

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Bibliographic Details
Published in:Metabolic brain disease 2021-10, Vol.36 (7), p.1445-1467
Main Authors: Ryan, Fari, Khoshnam, Seyed Esmaeil, Khodagholi, Fariba, Ashabi, Ghorbangol, Ahmadiani, Abolhassan
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Biochemistry
Biomedical and Life Sciences
Biomedicine
Cell activation
Cell Death
Cytosol - physiology
Endoplasmic Reticulum - physiology
Golgi Apparatus - physiology
Humans
Inflammation
Ischemia
Ischemic Stroke - complications
Ischemic Stroke - etiology
Ischemic Stroke - pathology
Metabolic Diseases
Mortality
Neuroinflammatory Diseases - etiology
Neuroinflammatory Diseases - prevention & control
Neurological diseases
Neurology
Neurons - pathology
Neurosciences
NLR Family, Pyrin Domain-Containing 3 Protein - physiology
Oncology
Organelles
Organelles - physiology
Pathogenesis
Peroxisomes - physiology
Review Article
Ribosomes - physiology
Stroke
Structural response
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Summary:Ischemic stroke is the second leading cause of mortality and disability globally. Neuronal damage following ischemic stroke is rapid and irreversible, and eventually results in neuronal death. In addition to activation of cell death signaling, neuroinflammation is also considered as another pathogenesis that can occur within hours after cerebral ischemia. Under physiological conditions, subcellular organelles play a substantial role in neuronal functionality and viability. However, their functions can be remarkably perturbed under neurological disorders, particularly cerebral ischemia. Therefore, their biochemical and structural response has a determining role in the sequel of neuronal cells and the progression of disease. However, their effects on cell death and neuroinflammation, as major underlying mechanisms of ischemic stroke, are still not understood. This review aims to provide a comprehensive overview of the contribution of each organelle on these pathological processes after ischemic stroke.
ISSN:0885-7490
1573-7365
DOI:10.1007/s11011-021-00770-z