Objective: This manuscript aimed to provide a comprehensive overview of the physiological, molecular, and cellular mechanisms triggered by reactive astrocytes (RA) in the context of spinal cord injury (SCI), with a particular focus on cases involving hyperglycaemia.
Methods: The compilation of articles related to astrocyte responses in neuropathological conditions, with a specific emphasis on those related to SCI and hyperglycaemia, was conducted by searching through databases including Science Direct, Web of Science, and PubMed.
Results And Conclusions: This article explores the dual role of astrocytes in both neurophysiological and neurodegenerative conditions within the central nervous system (CNS). In the aftermath of SCI and hyperglycaemia, astrocytes undergo a transformation into RA, adopting a distinct phenotype. While there are currently no approved therapies for SCI, various therapeutic strategies have been proposed to alleviate the detrimental effects of RAs following SCI and hyperglycemia. These strategies show promising potential in the treatment of SCI and its likely comorbidities.
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http://dx.doi.org/10.1080/13813455.2023.2264538 | DOI Listing |
Neurochem Res
January 2025
Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
In recent decades, researchers and clinicians have increasingly focused on glial cell function. One of the primary mechanisms influencing these functions is through extracellular vesicles (EVs), membrane-bound particles released by cells that are essential for intercellular communication. EVs can be broadly categorized into four main types based on their size, origin, and biogenesis: large EVs, small EVs (sEVs), autophagic EVs, and apoptotic bodies.
View Article and Find Full Text PDFFront Cell Neurosci
January 2025
Faculty of Chinese Medicine and State Key Laboratory of Quality Research in Chinese Medicines, Macau University of Science and Technology, Macau, Macao SAR, China.
Objective: Depression is a mental disorder that significantly impairs both physical and mental health. Recent studies have shown that reactive astrogliosis have gained significant attention for their involvement in the pathophysiology of depression. However, there is no bibliometric analysis in this research field.
View Article and Find Full Text PDFNat Neurosci
January 2025
Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany.
Our understanding of Alzheimer's disease (AD) has transformed from a purely neuronal perspective to one that acknowledges the involvement of glial cells. Despite remarkable progress in unraveling the biology of microglia, astrocytes and vascular elements, the exploration of oligodendrocytes in AD is still in its early stages. Contrary to the traditional notion of oligodendrocytes as passive bystanders in AD pathology, emerging evidence indicates their active participation in and reaction to amyloid and tau pathology.
View Article and Find Full Text PDFRedox Biol
January 2025
Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, 68198-5880, USA. Electronic address:
Methamphetamine is a widely abused drug associated with significant neuroinflammation and neurodegeneration, mainly through the activation of glial cells and neurons in the central nervous system. This study investigates the role of the astrocyte-specific NOD-like receptor family pyrin domain-containing protein 6 (NLRP6) inflammasome in methamphetamine-induced astrocytic pyroptosis and neuroinflammation. Our findings demonstrate that methamphetamine exposure induces NLRP6-dependent pyroptosis, astrocyte activation, and the release of proinflammatory cytokines in mouse primary astrocytes.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Department of Neurology, Division of Neuroimmunology, School of Medicine, Johns Hopkins University, Baltimore, MD, 21287, USA.
Chronic innate immune activation in the central nervous system (CNS) significantly contributes to neurodegeneration in progressive multiple sclerosis (MS). Using multiple experimental autoimmune encephalomyelitis (EAE) models, we discovered that NLRX1 protects neurons in the anterior visual pathway from inflammatory neurodegeneration. We quantified retinal ganglion cell (RGC) density and optic nerve axonal degeneration, gliosis, and T-cell infiltration in Nlrx1 and wild-type (WT) EAE mice and found increased RGC loss and axonal injury in Nlrx1 mice compared to WT mice in both active immunization EAE and spontaneous opticospinal encephalomyelitis (OSE) models.
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