ArticleNature communications2025
Loss of CFHR5 function reduces the risk for age-related macular degeneration.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed.
- Decoding the Factor H-Related Proteins: Gatekeepers of Complement Dysregulation in AMD.European journal of immunology · 2026Review
- Five tenets for advancing evidence-based precision medicine.Nature medicine · 2026Review
- Identification of novel blood-borne soluble binding partners of factor H-related proteins.Scientific reports · 2026Article
- CTx001 for Geographic Atrophy: A Gene Therapy Expressing Soluble, Truncated Complement Receptor 1 (Mini-CR1).Ophthalmology science · 2026Article
- A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.Frontiers in immunology · 2026Review
- Artificial intelligence for precision therapeutics in age-related macular degeneration: current advances, challenges, and future directions.Frontiers in artificial intelligence · 2026Review
- Article
- Factor-H-related protein 1 (FHR1), a promotor of para-inflammation in age-related macular degeneration.Journal of neuroinflammation · 2025Article
Corrections and comments
- Update ofLoss of2024
Authors and funding
21 authors.
Funding
Abstract
Age-related macular degeneration (AMD) is a prevalent cause of vision loss in the elderly with limited therapeutic options. A single chromosomal region around the complement factor H gene (CFH) is reported to explain nearly 25% of genetic AMD risk. Here, we used association testing, statistical finemapping and conditional analyses in 12,495 AMD cases and 461,686 controls to deconvolute four major CFH haplotypes that convey protection from AMD. We show that beyond CFH, two of these are explained by Finn-enriched frameshift and missense variants in the CFH modulator CFHR5. We demonstrate through a FinnGen sample recall study that CFHR5 variant carriers exhibit dose-dependent reductions in serum levels of the CFHR5 gene product FHR-5 and two functionally related proteins at the locus. Genetic reduction in FHR-5 correlates with higher complement activation capacity and a thicker retinal photoreceptor layer. Our results propose therapeutic downregulation of FHR-5 as promising to prevent or treat AMD.
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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.