ArticleThe American journal of pathology2015
Expression of human complement factor H prevents age-related macular degeneration-like retina damage and kidney abnormalities in aged Cfh knockout mice.
Article in The American journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 66 citations in OpenAlex.
- STING activation induces polarized cytokine secretion of IFN-β and IL-17A promoting photoreceptor death and choroidal disruption in age-related macular degeneration.Cell death & disease · 2026Article
- REECAP: Contrastive learning of retinal aging reveals genetic loci linking morphology to eye disease.medRxiv : the preprint server for health sciences · 2025Article
- Truncated complement factor H Y402 gene therapy rescues C3 glomerulonephritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Friend or foe: assessing the value of animal models for facilitating clinical breakthroughs in complement research.The Journal of clinical investigation · 2025Review
- Rodent Models of Retinal Degeneration: From Purified Cells in Culture to Living Animals.Cold Spring Harbor perspectives in medicine · 2024Review
- Seeding activity of human superoxide dismutase 1 aggregates in familial and sporadic amyotrophic lateral sclerosis postmortem neural tissues by real-time quaking-induced conversion.Acta neuropathologica · 2024Article
- Gliosis-dependent expression of complement factor H truncated variants attenuates retinal neurodegeneration following ischemic injury.Journal of neuroinflammation · 2024Article
- Fluorescence Lifetime Imaging Ophthalmoscopy of Mouse Models of Age-related Macular Degeneration.Translational vision science & technology · 2024Article
- The human factor H protein family - an update.Frontiers in immunology · 2024Review
- Polarized Desmosome and Hemidesmosome Shedding via Small Extracellular Vesicles is an Early Indicator of Outer Blood-Retina Barrier Dysfunction.Journal of extracellular biology · 2023Article
- AAV Gene Augmentation of Truncated Complement Factor H Differentially Rescues Ocular Complement Dysregulation in a Mouse Model.Investigative ophthalmology & visual science · 2023Article
- A Protocol to Evaluate and Quantify Retinal Pigmented Epithelium Pathologies in Mouse Models of Age-Related Macular Degeneration.Journal of visualized experiments : JoVE · 2023Article
- Contribution of animal models to the mechanistic understanding of Alternative Pathway and Amplification Loop (AP/AL)-driven Complement-mediated Diseases.Immunological reviews · 2023Review
- Local factor H production by human choroidal endothelial cells mitigates complement deposition: implications for macular degeneration.The Journal of pathology · 2022Article
- Unravelling the therapeutic potential of IL-33 for atrophic AMD.Eye (London, England) · 2022Review
- CFH Loss in Human RPE Cells Leads to Inflammation and Complement System Dysregulation via the NF-κB Pathway.International journal of molecular sciences · 2021Article
- Murine Factor H Co-Produced in Yeast With Protein Disulfide Isomerase Ameliorated C3 Dysregulation in Factor H-Deficient Mice.Frontiers in immunology · 2021Article
- Modulation of Tmem135 Leads to Retinal Pigmented Epithelium Pathologies in Mice.Investigative ophthalmology & visual science · 2020Article
- High-density lipoproteins are a potential therapeutic target for age-related macular degeneration.The Journal of biological chemistry · 2020Article
- Central Role of Oxidative Stress in Age-Related Macular Degeneration: Evidence from a Review of the Molecular Mechanisms and Animal Models.Oxidative medicine and cellular longevity · 2020Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Complement factor H (CFH) is an important regulatory protein in the alternative pathway of the complement system, and CFH polymorphisms increase the genetic risk of age-related macular degeneration dramatically. These same human CFH variants have also been associated with dense deposit disease. To mechanistically study the function of CFH in the pathogenesis of these diseases, we created transgenic mouse lines using human CFH bacterial artificial chromosomes expressing full-length human CFH variants and crossed these to Cfh knockout (Cfh(-/-)) mice. Human CFH protein inhibited cleavage of mouse complement component 3 and factor B in plasma and in retinal pigment epithelium/choroid/sclera, establishing that human CFH regulates activation of the mouse alternative pathway. One of the mouse lines, which express relatively higher levels of CFH, demonstrated functional and structural protection of the retina owing to the Cfh deletion. Impaired visual function, detected as a deficit in the scotopic electroretinographic response, was improved in this transgenic mouse line compared with Cfh(-/-) mice, and transgenics had a thicker outer nuclear layer and less sub-retinal pigment epithelium deposit accumulation. In addition, expression of human CFH also completely protected the mice from developing kidney abnormalities associated with loss of CFH. These humanized CFH mice present a valuable model for study of the molecular mechanisms of age-related macular degeneration and dense deposit disease and for testing therapeutic targets.
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