ArticleNature communications2024
Levels of complement factor H-related 4 protein do not influence susceptibility to age-related macular degeneration or its course of progression.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 11 citations in OpenAlex.
- Decoding the Factor H-Related Proteins: Gatekeepers of Complement Dysregulation in AMD.European journal of immunology · 2026Review
- Identification of novel blood-borne soluble binding partners of factor H-related proteins.Scientific reports · 2026Article
- Choriocapillaris Flow Signal Deficits Are Associated With AMD Onset and Early Progression Over Three Years: ALSTAR2 Follow-Up.Investigative ophthalmology & visual science · 2026Article
- A new perspective on AMD pathogenesis: a sequential Factor H-centered view of complement dysregulation.Frontiers in immunology · 2026Review
- CTx001 for Geographic Atrophy: A Gene Therapy Expressing Soluble, Truncated Complement Receptor 1 (Mini-CR1).Ophthalmology science · 2026Article
- Factor-H-related protein 1 (FHR1), a promotor of para-inflammation in age-related macular degeneration.Journal of neuroinflammation · 2025Article
- Loss of CFHR5 function reduces the risk for age-related macular degeneration.Nature communications · 2025Article
- Genetic Associations of Rod- and Cone-Mediated Vision in Aging and Age-Related Macular Degeneration.Investigative ophthalmology & visual science · 2025Article
- Rare predicted loss-of-function and damaging missense variants in CFHR5 associate with protection from age-related macular degeneration.American journal of human genetics · 2025Article
- Modeling complex age-related eye disease.Progress in retinal and eye research · 2024Review
Corrections and comments
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Authors and funding
15 authors at 1 institution in 1 country.
Funding
Abstract
Dysregulation of the alternative pathway (AP) of the complement system is a significant contributor to age-related macular degeneration (AMD), a primary cause of irreversible vision loss worldwide. Here, we assess the contribution of the liver-produced complement factor H-related 4 protein (FHR-4) to AMD initiation and course of progression. We show that FHR-4 variation in plasma and at the primary location of AMD-associated pathology, the retinal pigment epithelium/Bruch's membrane/choroid interface, is entirely explained by three independent quantitative trait loci (QTL). Using two distinct cohorts composed of a combined 14,965 controls and 20,741 cases, we ascertain that independent QTLs for FHR-4 are distinct from variants causally associated with AMD, and that FHR-4 variation is not independently associated with disease. Additionally, FHR-4 does not appear to influence AMD progression course among patients with disease driven predominantly by AP dysregulation. Modulation of FHR-4 is therefore unlikely to be an effective therapeutic strategy for 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 Socratic graph.