ReviewInternational journal of retina and vitreous2022
C1q and the classical complement cascade in geographic atrophy secondary to age-related macular degeneration.
Review in International journal of retina and vitreous, 2022. 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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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Pharmacological Characterization of a Novel Complement C3 Inhibitor Antibody Fragment.Ophthalmology and therapy · 2026Article
- Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Complement Inhibition in Geographic Atrophy: Clinical Evidence for Pegcetacoplan and Avacincaptad Pegol.Cureus · 2026Review
- Persistent microglial activation following neonatal CMV infection mediates neurodegeneration.Science advances · 2026Article
- Systemic inflammation triggers local complement production in the mouse retina and RPE.Journal of neuroinflammation · 2026Article
- Complement in brain and eye disease: shared mechanisms, convergent pathologies, and common therapeutic opportunities.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Dysfunction of Unc119, a Transducin-Binding Protein, Leads to Cone-Rod Dystrophy through Activating JAK-Stat and NF-κB Inflammatory Pathways in the Mouse Retina.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Retinal biomarkers in schizophrenia spectrum disorders: evidence and implications for the neurodevelopmental and neurodegenerative models.Frontiers in medicine · 2025Review
- The Role of Reactive Oxygen Species in Age-Related Macular Degeneration: A Comprehensive Review of Antioxidant Therapies.Biomedicines · 2024Review
- The Complement System as a Therapeutic Target in Retinal Disease.Medicina (Kaunas, Lithuania) · 2024Review
- Recent Advances in Our Understanding of Age-Related Macular Degeneration: Mitochondrial Dysfunction, Redox Signaling, and the Complement System.Aging and disease · 2024Review
- Dysregulated C1q and CD47 in the aging monkey brain: association with myelin damage, microglia reactivity, and cognitive decline.Frontiers in immunology · 2024Article
- C5 inhibitor avacincaptad pegol treatment for geographic atrophy: A comprehensive review.Immunotherapy · 2024Review
- Treating patients with geographic atrophy: are we there yet?International journal of retina and vitreous · 2023Review
- Sexually dimorphic extracellular vesicle responses after chronic spinal cord injury are associated with neuroinflammation and neurodegeneration in the aged brain.Journal of neuroinflammation · 2023Article
- Geographic atrophy: pathophysiology and current therapeutic strategies.Frontiers in ophthalmology · 2023Review
- Single-cell sequencing reveals an important role of SPP1 and microglial activation in age-related macular degeneration.Frontiers in cellular neuroscience · 2023Article
- Cochlear inflammaging: cellular and molecular players of the innate and adaptive immune system in age-related hearing loss.Frontiers in neurology · 2023Review
- Complement and local ocular inflammatory response: Chronic immune factors in myopia.Science progressReview
- Contributions of Lipid-Related Metabolites and Complement Proteins to Early and Intermediate Age-Related Macular Degeneration.Ophthalmology scienceArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Geographic atrophy (GA) secondary to age-related macular degeneration (AMD) is a retinal neurodegenerative disorder. Human genetic data support the complement system as a key component of pathogenesis in AMD, which has been further supported by pre-clinical and recent clinical studies. However, the involvement of the different complement pathways (classical, lectin, alternative), and thus the optimal complement inhibition target, has yet to be fully defined. There is evidence that C1q, the initiating molecule of the classical pathway, is a key driver of complement activity in AMD. C1q is expressed locally by infiltrating phagocytic cells and C1q-activating ligands are present at disease onset and continue to accumulate with disease progression. The accumulation of C1q on photoreceptor synapses with age and disease is consistent with its role in synapse elimination and neurodegeneration that has been observed in other neurodegenerative disorders. Furthermore, genetic deletion of C1q, local pharmacologic inhibition within the eye, or genetic deletion of downstream C4 prevents photoreceptor cell damage in mouse models. Hence, targeting the classical pathway in GA could provide a more specific therapeutic approach with potential for favorable efficacy and safety.
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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.