ArticleJournal of clinical medicine2020
Fructosamine-3-Kinase as a Potential Treatment Option for Age-Related Macular Degeneration.
Article in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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, 13 citations in OpenAlex.
- The molecular basis of Human FN3K mediated phosphorylation of glycated substrates.Nature communications · 2025Article
- Structural basis for FN3K-mediated protein deglycation.Structure (London, England : 1993) · 2024Article
- The molecular basis of Human FN3K mediated phosphorylation of glycated substrate.bioRxiv : the preprint server for biology · 2024Article
- Fructosyl Amino Oxidase as a Therapeutic Enzyme in Age-Related Macular Degeneration.International journal of molecular sciences · 2024Article
- Epigenetic meets metabolism: novel vulnerabilities to fight cancer.Cell communication and signaling : CCS · 2023Review
- Enzymatic Deglycation of Damaged Skin by Means of Combined Treatment of Fructosamine-3-Kinase and Fructosyl-Amino Acid Oxidase.International journal of molecular sciences · 2023Article
- Topical Application of Deglycating Enzymes as an Alternative Non-Invasive Treatment for Presbyopia.International journal of molecular sciences · 2023Article
- A Potential Role for Fructosamine-3-Kinase in Cataract Treatment.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Age-related macular degeneration is the leading cause of blindness in the developed world. Since advanced glycation end products (AGEs) are implicated in the pathogenesis of AMD through various lines of evidence, we investigated the potential of fructosamine-3-kinase (FN3K) in the disruption of retinal AGEs, drusenoid material and drusenoid lesions in patients with AMD. AGE-type autofluorescence was measured to evaluate the effects of FN3K on glycolaldehyde-induced AGE-modified neural porcine retinas and unmodified human neural retinas. Eye pairs from cigarette-smoke- and air-exposed mice were treated and evaluated histologically. Automated optical image analysis of human tissue sections was performed to compare control- and FN3K-treated drusen and near-infrared (NIR) microspectroscopy was performed to examine biochemical differences. Optical coherence tomography (OCT) was used to evaluate the effect of FN3K on drusenoid deposits after treatment of post-mortem human eyes. FN3K treatment provoked a significant decrease (41%) of AGE-related autofluorescence in the AGE-modified porcine retinas. Furthermore, treatment of human neural retinas resulted in significant decreases of autofluorescence (-24%). FN3K-treated murine eyes showed less drusenoid material. Pairwise comparison of drusen on tissue sections revealed significant changes in color intensity after FN3K treatment. NIR microspectroscopy uncovered clear spectral differences in drusenoid material (Bruch's membrane) and drusen after FN3K treatment. Ex vivo treatment strongly reduced size of subretinal drusenoid lesions on OCT imaging (up to 83%). In conclusion, our study demonstrated for the first time a potential role of FN3K in the disruption of AGE-related retinal autofluorescence, drusenoid material and drusenoid lesions in patients with AMD.
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Registered trials
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