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How Cytosolic Compartments Play Safeguard Functions Against Neuroinflammation and Cell Death in Cerebral Ischemia Publisher Pubmed



Ryan F1 ; Khoshnam SE2 ; Khodagholi F3 ; Ashabi G4 ; Ahmadiani A3
Authors
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Authors Affiliations
  1. 1. Centre for Research in Neuroscience, The Research Institute of the McGill University Health Centre, Montreal, QC, Canada
  2. 2. Persian Gulf Physiology Research Centre, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
  3. 3. Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  4. 4. Department of Physiology, Faculty of Medicine, Tehran University of Medical Sciences, PO Box: 1417613151, Tehran, Iran

Source: Metabolic Brain Disease Published:2021


Abstract

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. © 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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