ArticleAntioxidants (Basel, Switzerland)2025
Complement Receptor 3 Regulates Microglial Exosome Release and Related Neurotoxicity via NADPH Oxidase in Neuroinflammation Associated with Parkinson's Disease.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- The Versatile Roles of Exosomes in Neurodegenerative Disorders: From Pathological Mechanism and Diagnostic Biomarkers to Therapeutic Application.Drug design, development and therapy · 2026Review
- A Hypothesis of Gut-Liver Mediated Heterosis: Multi-Omics Insights into Hybrid Taimen Immunometabolism (Animals : an open access journal from MDPI · 2025Article
- Comparative Anatomical and Morphometric Analysis of Eustachian Tube Across Species.Audiology research · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Microglia-mediated chronic neuroinflammation is a common pathological feature of Parkinson's disease (PD). Strong evidence suggests that activated microglia can lesion neurons by releasing exosomes. However, the mechanisms of exosome release from activated microglia remain unclear. We recently revealed a key role of complement receptor 3 (CR3) in regulating microglial activation in the process of progressive neurodegeneration. This study aimed to investigate whether CR3 can regulate exosome release from activated microglia, as well as the underlying mechanisms. We found that LPS, an inducer of microglial M1 activation, induced exosome release from activated microglia. Inhibition of exosome synthesis suppressed LPS-induced microglial activation, gene expression of proinflammatory factors, and related neurotoxicity. Silencing or knocking out CR3 attenuated LPS-induced exosome release in microglia. NADPH oxidase (NOX2) was further identified as a downstream signal of CR3, mediating microglial exosome release and related neurotoxicity. CR3 silencing blocked LPS-induced NOX2 activation and superoxide production through inhibition of p47
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