Revisiting the role of factor H in age-related macular degeneration: Insights from complement-mediated renal disease and rare genetic variants
Open accessAbstract
Ophthalmologists are long familiar with the eye showing signs of systemic disease, but the association between age-related macular degeneration and abnormal complement activation, common to several renal disorders, has only recently been elucidated. Although complement activation products were identified in drusen almost three decades ago, it was not until the early 21st century that a single-nucleotide polymorphism in the complement factor H gene was identified as a major heritable determinant of age-related macular degeneration, galvanizing global efforts to unravel the pathogenesis of this common disease. Advances in proteomic analyses and familial aggregation studies have revealed distinctive clinical phenotypes segregated by the functional effects of common and rare genetic variants on the mature protein and its splice variant, factor H-like protein 1. The predominance of loss-of-function, N-terminal mutations implicate age-related macular degeneration as a disease of general complement dysregulation, offering several therapeutic avenues for its modulation. Here, we explore the molecular impact of these mutations/polymorphisms on the ability of variant factor H/factor H-like protein 1 to localize to polyanions, pentraxins, proinflammatory triggers, and cell surfaces across ocular and renal tissues and exert its multimodal regulatory functions and their clinical implications. Finally, we critically evaluate key therapeutic and diagnostic efforts in this rapidly evolving field.
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Most complement proteins are produced in the liver, while others (C1q, C7, Factor D, and properdin) are produced at extrahepatic sites by various cells, including monocytes, macrophages, and glial and endothelial cells.
“While most complement proteins are produced in the liver, others (such as C1q, C7, Factor D, and properdin) are produced at extrahepatic sites by various cells, including monocytes, macrophages, and glial and endothelial cells [7,204,205].”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [7]
The kidney and eye are known to be susceptible to complement dysregulation.
“and are known to be susceptible to complement dysregulation [7,209].”
From Bruch’s Membrane: A Key Consideration with Complement-Based Therapies for Age-Related Macular Degeneration (2023) · cites this paper as [7]
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Rare Complement Factor H Variant Associated With Age-Related Macular Degeneration in the Amish
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Hammadi, S., Tzoumas, N., Ferrara, M., Meschede, I. P., Lo, K., Harris, C., Lako, M., & Steel, D. H. (2023) · Journal of Clinical Medicine · doi:10.3390/jcm12082870 · Cited by 44 · see citing works
Self-citationComplement inhibitors for age-related macular degeneration
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Self-citationTzoumas, N., Kavanagh, D., Cordell, H. J., Lotery, A. J., Patel, P. J., & Steel, D. H. (2022) · Human Molecular Genetics · doi:10.1093/hmg/ddac060 · Cited by 31 · see citing works
Self-citation
- Authors
- Tzoumas, N., Hallam, D., Harris, C. L., Lako, M., Kavanagh, D., & Steel, D. H. W.
- Affiliations
- Newcastle University (GB)
- Royal Victoria Infirmary (GB)
- Sunderland Eye Infirmary (GB)
- Corresponding author
- Tzoumas, Nikolaos
- Venue
- Survey of Ophthalmology
- Publisher
- Elsevier BV
- Published
- 2021-03
- Volume
- 66
- Issue
- 2
- Pages
- 378-401
- ISSN
- 0039-6257 (ISSN-L)
- OpenAlex
- W3095970076
- Cited by
- 33
- References
- 266
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 7 · 2023: 7 · 2022: 5 · 2021: 7
- FWCI
- 0.46
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Survey of Ophthalmology (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Macular Society
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Ocular Diseases and Behçet’s Syndrome
- Keywords
- complement factor H, age-related macular degeneration, complement activation, complement dysregulation, factor H-like protein 1, single nucleotide polymorphisms, rare variants, loss-of-function mutations, drusen, pentraxins, polyanions, complement regulation, therapeutic target, diagnosis
- MeSH terms
- Complement System Proteins, Humans, Macular Degeneration, Phenotype, Complement Factor H, Proteomics
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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