ArticleInvestigative ophthalmology & visual science2025
Elevated Plasma Complement Factors in CRB1-Associated Inherited Retinal Dystrophies.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Tyrosine Kinase Receptors, Inhibition, and Potential Role in the Pharmacotherapy of Retinal Disorders.Ophthalmology and therapy · 2026Review
- Prediction of Postoperative Length of Stay in Patients with Hip Fracture: A Two-Stage Machine Learning Approach.Healthcare informatics research · 2026Article
- Machine Learning-Based Classification of Active and Latent Phases of Inherited Retinal Dystrophies Using Synthetic Proteomic Data: A Pathway-Based Application Exercise.Healthcare informatics research · 2026Article
- Pathogenicity Analysis of Two Novel CRB1 Mutations in Three Chinese Inherited Retinal Dystrophy Families and a Literature Review.Translational vision science & technology · 2026Review
- Bile Acid Metabolism Changes in Patients with aOphthalmology scienceArticle
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Authors and funding
34 authors.
Funding
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Abstract
Purpose: To determine the profile of inflammation-related proteins and complement system factors in the plasma of CRB1-associated inherited retinal dystrophies (CRB1-IRDs). Methods: We used the Olink Explore 384 Inflammation II panel for targeted proteomics in 30 cases and 29 controls (cohort I) to identify immune pathways involved in CRB1-IRDs. Genotyping was performed in cohort I and a second cohort of 123 patients from 14 countries and 1292 controls (cohort II). Results: A significant shift in complement cascade factors was observed in plasma proteomes of CRB1-IRD patients (enrichment for complement cascade, Padj = 3.03 × 10-15). We detected higher plasma levels of complement factor I and complement factor H [CFH] (q = 0.008 and q = 0.046, respectively, adjusted for age and sex), inhibitors of complement component 3 (C3), which correlated significantly (Pearson's coefficient >0.6) with elevated levels of C3 (q = 0.064). The CRB1 missense variants frequently found in patients showed a strong linkage disequilibrium with the common CFH variant rs7535263 (D' = 0.97 for p.(Cys948Tyr); D' = 1.0 for p.(Arg764Cys)), known to be linked with altered plasma CFH-related protein levels. Correction for the CFH genotype revealed significantly elevated plasma levels of CFH-related 2 (CFHR2) in CRB1-IRD patients (q = 0.041). Conclusions: CRB1-IRDs are characterized by changes in plasma levels of complement factors and proteins of the innate immune system, and linkage between CRB1 and CFH genes implicates functional variants of the CFH-CFHR locus with specific pathogenic variants of CRB1.
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