ReviewSeminars in immunopathology2018
The eye as a complement dysregulation hotspot.
Review in Seminars in immunopathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 105 citations in OpenAlex.
- Complement family member CFI polymorphisms and AMD susceptibility from a comprehensive analysis.Bioscience reports · 2020Pooled it
- Diagnostic interpretation of CFH expression in pan-cancer analyses: the importance of factor H-like 1 isoform resolution.BMC cancer · 2026Article
- Pharmacological Characterization of a Novel Complement C3 Inhibitor Antibody Fragment.Ophthalmology and therapy · 2026Article
- ApoE- and Cfh-deficient mice exhibit structural and molecular features of human early-intermediate retinal degeneration.Animal models and experimental medicine · 2026Article
- Decoding the Factor H-Related Proteins: Gatekeepers of Complement Dysregulation in AMD.European journal of immunology · 2026Review
- C3a and C5a plasma concentrations in patients with diabetic retinopathy: a cross-sectional study.International journal of retina and vitreous · 2026Article
- Molecular Crosstalk in Age-Related Macular Degeneration: Integrating Oxidative Stress, Inflammation, microRNAs, and Genetic Susceptibility Toward Precision Therapeutics.Biomolecules · 2026Review
- High throughput tear proteomics with data independent acquisition enables biomarker discovery in allergic conditions.Scientific reports · 2025Article
- Article
- Restoring Glutathione Homeostasis in Glycation-Related Eye Diseases: Mechanistic Insights and Therapeutic Interventions Beyond VEGF Inhibition.Antioxidants (Basel, Switzerland) · 2025Review
- The role of complement factor I rare genetic variants in age related macular degeneration in Finland.Human molecular genetics · 2025Article
- Dynamic Complement Protein Changes in Aqueous Humor and Plasma of Patients With Retinal Vein Occlusion During Ranibizumab Treatment.Journal of inflammation research · 2025Article
- Intraocular complement activation is independent of systemic complement activation and is related to macular vascular remodelling in retinal vein occlusion.BMC ophthalmology · 2024Article
- Complement regulation in the eye: implications for age-related macular degeneration.The Journal of clinical investigation · 2024Review
- Complement Suppresses the Initial Type 1 Interferon Response to Ocular Herpes Simplex Virus Type 1 Infection in Mice.Pathogens (Basel, Switzerland) · 2024Article
- The Relationship between Complements and Age-Related Macular Degeneration and Its Pathogenesis.Journal of ophthalmology · 2024Review
- Role of Complement in the Onset of Age-Related Macular Degeneration.Biomolecules · 2023Review
- Delivery Systems in Ocular Retinopathies: The Promising Future of Intravitreal Hydrogels as Sustained-Release Scaffolds.Pharmaceutics · 2023Review
- Article
- Proteomics profiling of vitreous humor reveals complement and coagulation components, adhesion factors, and neurodegeneration markers as discriminatory biomarkers of vitreoretinal eye diseases.Frontiers in immunology · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Complement turnover is tightly regulated throughout the human body in order to prevent over-activation and subsequent damage from inflammation. In the eye, low-level complement activation is maintained to provide immune tolerance in this immune privileged organ. Conversely, the complement system is suppressed in the cornea to protect it from continuous immunological insult. Over-activation of the complement cascade has been implicated in the disease progression of glaucoma and diabetic retinopathy and is now known to be a central driver in the pathogenesis of age-related macular degeneration (AMD). Indeed, it is with AMD where the most recent and exciting work has been carried out with complement-based therapies entering into clinical trials. However, the success of these trials will depend upon delivering the therapeutics to the correct anatomical sites within the eye, so a full understanding of how complement regulation is compartmentalized in the eye is required, a topic that will be highlighted in this review.
Indexed as
Identifiers
What OpenQuestion holds
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.