The role of Galectin-3/MAC-2 in the activation of the innate-immune function of phagocytosis in microglia in injury and disease
Journal of Molecular Neuroscience, ISSN: 0895-8696, Vol: 39, Issue: 1-2, Page: 99-103
2009
- 98Citations
- 87Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations98
- Citation Indexes98
- 98
- CrossRef87
- Captures87
- Readers87
- 87
Review Description
Microglia are a self-sustained population of immune/myeloid cells present throughout the central nervous system (CNS). Microglia are in a "resting" state in the normal adult CNS. They turn "active" in injury and disease (e.g., trauma, neurodegeneration, and infection). Activated microglia can be beneficial as well as detrimental/neurotoxic. The innate-immune function of phagocytosis of tissue debris, neurotoxic factor, and pathogens is a beneficial function of microglia. The current manuscript reviews the role of Galectin-3 (known also as MAC-2; Galectin-3/MAC-2) in the activation of the phagocytosis of degenerated myelin that is mediated by complement receptor-3 (known also as MAC-1; CD11b/CD18; αMβ2 integrin) and SRA (scavenger receptor-AI/II). Observations suggest that Galectin-3/MAC-2 may act as a molecular switch that activates phagocytosis by up-regulating and prolonging KRas-GTP-dependent PI3K (phosphatidylinositol 3-kinase) activity. A similar mechanism may regulate the phagocytosis of other tissue debris, neurotoxic factors and pathogens in neurodegenerative and infectious diseases. © Humana Press 2009.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=74149092361&origin=inward; http://dx.doi.org/10.1007/s12031-009-9186-7; http://www.ncbi.nlm.nih.gov/pubmed/19253007; http://link.springer.com/10.1007/s12031-009-9186-7; https://dx.doi.org/10.1007/s12031-009-9186-7; https://link.springer.com/article/10.1007/s12031-009-9186-7; http://www.springerlink.com/index/10.1007/s12031-009-9186-7; http://www.springerlink.com/index/pdf/10.1007/s12031-009-9186-7
Springer Science and Business Media LLC
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