ReviewInternational journal of molecular sciences2020
Control of Innate Immunity by Sialic Acids in the Nervous Tissue.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 45 citations in OpenAlex.
- St6gal1-mediated sialylation protects retinal ganglion cells by restraining microglial phagocytosis.Journal of neuroinflammation · 2026Article
- When glycobiology meets inflammasome activation: Insights and implications.Journal of advanced research · 2026Review
- Modified AAV5 capsid for improved brain biodistribution following direct injection in preclinical models.Molecular therapy. Methods & clinical development · 2025Article
- The role of inhibitory immune checkpoint receptors in the pathogenesis of Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Catastrophic selection: the other side of the coin.Annals of medicine · 2024Article
- Hyperglycosylation as an Indicator of Aging in the Bone Metabolome ofMetabolites · 2024Article
- Complement C1q-mediated microglial synaptic elimination by enhancing desialylation underlies sevoflurane-induced developmental neurotoxicity.Cell & bioscience · 2024Article
- The alteration and role of glycoconjugates in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- The role of sialidases in the pathogenesis of bacterial vaginosis and their use as a promising pharmacological target in bacterial vaginosis.Frontiers in cellular and infection microbiology · 2024Review
- Role of Xenosialylation in Post-Infectious and Post-Vaccination Complications, Including Covid-19 and Anti-SARS-CoV-2 Vaccination.Journal of inflammation research · 2024Article
- Neuroprotective role of sialic-acid-binding immunoglobulin-like lectin-11 in humanized transgenic mice.Frontiers in neuroscience · 2024Article
- Sialic Acid Mimetic Microglial Sialic Acid-Binding Immunoglobulin-like Lectin Agonism: Potential to Restore Retinal Homeostasis and Regain Visual Function in Age-Related Macular Degeneration.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Sialic acid metabolism orchestrates transcellular connectivity and signaling in glioblastoma.Neuro-oncology · 2023Article
- Increased α-2,6 sialic acid on microglia in amyloid pathology is resistant to oseltamivir.GeroScience · 2023Article
- CD33/TREM2 Signaling Mediates Sleep Deprivation-Induced Memory Impairment by Regulating Microglial Phagocytosis.Neuromolecular medicine · 2023Article
- 6'-sialyllactose ameliorates the ototoxic effects of the aminoglycoside antibiotic neomycin in susceptible mice.Frontiers in immunology · 2023Article
- Article
- The CD33 short isoform is a gain-of-function variant that enhances AβMolecular neurodegeneration · 2021Article
- Polysialic Acid in the Immune System.Frontiers in immunology · 2021Review
- Comprehensive Proteomic Profiling of Urinary Exosomes and Identification of Potential Non-invasive Early Biomarkers of Alzheimer's Disease in 5XFAD Mouse Model.Frontiers in genetics · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Sialic acids (Sias) are the most abundant terminal sugar residues of glycoproteins and glycolipids on the surface of mammalian cells. The nervous tissue is the organ with the highest expression level of Sias. The 'sialylation' of glycoconjugates is performed via sialyltransferases, whereas 'desialylation' is done by sialidases or is a possible consequence of oxidative damage. Sialic acid residues on the neural cell surfaces inhibit complement and microglial activation, as well as phagocytosis of the underlying structures, via binding to (i) complement factor H (CFH) or (ii) sialic acid-binding immunoglobulin-like lectin (SIGLEC) receptors. In contrast, activated microglial cells show sialidase activity that desialylates both microglia and neurons, and further stimulates innate immunity via microglia and complement activation. The desialylation conveys neurons to become susceptible to phagocytosis, as well as triggers a microglial phagocytosis-associated oxidative burst and inflammation. Dysfunctions of the 'Sia-SIGLEC' and/or 'Sia-complement' axes often lead to neurological diseases. Thus, Sias on glycoconjugates of the intact glycocalyx and its desialylation are major regulators of neuroinflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.