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Fructosyl Amino Oxidase as a Therapeutic Enzyme in Age-Related Macular Degeneration

International Journal of Molecular Sciences, ISSN: 1422-0067, Vol: 25, Issue: 9
2024
  • 1
    Citations
  • 0
    Usage
  • 8
    Captures
  • 2
    Mentions
  • 0
    Social Media
Metric Options:   Counts1 Year3 Year

Metrics Details

  • Citations
    1
    • Patent Family Citations
      1
      • Patent Families
        1
  • Captures
    8
  • Mentions
    2
    • Blog Mentions
      1
      • Blog
        1
    • News Mentions
      1
      • News
        1

Most Recent News

Researchers from Ghent University Discuss Research in Age-Related Macular Degeneration (Fructosyl Amino Oxidase as a Therapeutic Enzyme in Age-Related Macular Degeneration)

2024 MAY 27 (NewsRx) -- By a News Reporter-Staff News Editor at Pain & Central Nervous System Daily News -- New study results on age-related

Article Description

Age-related macular degeneration (AMD) is an age-related disorder that is a global public health problem. The non-enzymatic Maillard reaction results in the formation of advanced glycation end products (AGEs). Accumulation of AGEs in drusen plays a key role in AMD. AGE-reducing drugs may contribute to the prevention and treatment of AGE-related disease. Fructosamine oxidase (FAOD) acts on fructosyl lysine and fructosyl valine. Based upon the published results of fructosamine 3-kinase (FN3K) and FAOD obtained in cataract and presbyopia, we studied ex vivo FAOD treatment as a non-invasive AMD therapy. On glycolaldehyde-treated porcine retinas, FAOD significantly reduced AGE autofluorescence (p = 0.001). FAOD treatment results in a breakdown of AGEs, as evidenced using UV fluorescence, near-infrared microspectroscopy on stained tissue sections of human retina, and gel permeation chromatography. Drusen are accumulations of AGEs that build up between Bruch’s membrane and the retinal pigment epithelium. On microscopy slides of human retina affected by AMD, a significant reduction in drusen surface to 45 ± 21% was observed following FAOD treatment. Enzymatic digestion followed by mass spectrometry of fructose- and glucose-based AGEs (produced in vitro) revealed a broader spectrum of substrates for FAOD, as compared to FN3K, including the following: fructosyllysine, carboxymethyllysine, carboxyethyllysine, and imidazolone. In contrast to FN3K digestion, agmatine (4-aminobutyl-guanidine) was formed following FAOD treatment in vitro. The present study highlights the therapeutic potential of FAOD in AMD by repairing glycation-induced damage.

Bibliographic Details

Delanghe, Joris R; Diana Di Mavungu, Jose; Beerens, Koen; Himpe, Jonas; Bostan, Nezahat; Speeckaert, Marijn M; Vrielinck, Henk; Vral, Anne; Van Den Broeke, Caroline; Huizing, Manon; Van Aken, Elisabeth

MDPI AG

Chemical Engineering; Biochemistry, Genetics and Molecular Biology; Chemistry; Computer Science

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