ArticleFrontiers in neuroscience2022
Complement C3a receptor inactivation attenuates retinal degeneration induced by oxidative damage.
Article in Frontiers in neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Human retinal organoids for modelling dry age-related macular degeneration and screening drugs.Genes & diseases · 2025Article
- Complement C3/C3aR Signaling Pathway Inhibition Ameliorates Retinal Damage in Experimental Retinal Vein Occlusion.Investigative ophthalmology & visual science · 2025Article
- Elevated Plasma Complement Factors in CRB1-Associated Inherited Retinal Dystrophies.Investigative ophthalmology & visual science · 2025Article
- Complement C3 knockout protects photoreceptors in the sodium iodate model.Experimental eye research · 2025Article
- C3AR1 may aggravate diabetic nephropathy by mediating oxidative stress via ITGB2 regulation in renal tubular epithelial cells.PloS one · 2025Article
- Dual role of complement in neuronal repair.Frontiers in immunology · 2025Review
- The Complement System as a Therapeutic Target in Retinal Disease.Medicina (Kaunas, Lithuania) · 2024Review
- Decitabine improves MMS-induced retinal photoreceptor cell damage by targeting DNMT3A and DNMT3B.Frontiers in molecular neuroscience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal degeneration causes vision loss and threatens the health of elderly individuals worldwide. Evidence indicates that the activation of the complement system is associated with retinal degeneration. However, the mechanism of complement signaling in retinal degeneration needs to be further studied. In this study, we show that the expression of C3 and C3a receptor (C3ar1) is positively associated with the inflammatory response and retinal degeneration. Genetic deletion of C3 and pharmacological inhibition of C3ar1 resulted in the alleviation of neuroinflammation, prevention of photoreceptor cell apoptosis and restoration of visual function. RNA sequencing (RNA-seq) identified a C3ar1-dependent network shown to regulate microglial activation and astrocyte gliosis formation. Mechanistically, we found that STAT3 functioned downstream of the C3-C3ar1 pathway and that the C3ar1-STAT3 pathway functionally mediated the immune response and photoreceptor cell degeneration in response to oxidative stress. These findings reveal an important role of C3ar1 in oxidative-induced retinal degeneration and suggest that intervention of the C3ar1 pathway may alleviate retinal degeneration.
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Registered trials
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