Publications by authors named "Ramona Rudnick"
Article Synopsis
- Genetic variants in complement factor H (CFH) have been linked to age-related macular degeneration (AMD) by affecting CFH's ability to bind to modified self-ligands like malondialdehyde (MDA), disrupting complement regulation.
- A genome-wide study found specific genetic variants, such as rs1061170 and certain deletions, that influence CFH and its splice variant FHL-1’s binding capabilities to MDA in healthy individuals.
- FHR1 and FHR3 were identified as competitive binders that can inhibit CFH's function on MDA-modified surfaces, leading to increased complement activation and suggesting that specific genetic variations offer protection against AMD by improving tissue homeostasis.
Defective complement action is a cause of several human glomerular diseases including atypical hemolytic uremic syndrome (aHUS), anti-neutrophil cytoplasmic antibody mediated vasculitis (ANCA), C3 glomerulopathy, IgA nephropathy, immune complex membranoproliferative glomerulonephritis, ischemic reperfusion injury, lupus nephritis, membranous nephropathy, and chronic transplant mediated glomerulopathy. Here we summarize ongoing clinical trials of complement inhibitors in nine glomerular diseases and show which inhibitors are used in trials for these renal disorders (http://clinicaltrials.gov).
View Article and Find Full Text PDFFactor H related-protein 5 (CFHR5) is a surface-acting complement activator and variations in the CFHR5 gene are linked to CFHR glomerulonephritis. In this study, we show that FHR5 binds to laminin-521, the major constituent of the glomerular basement membrane, and to mesangial laminin-211. Furthermore, we identify malondialdehyde-acetaldehyde (MAA) epitopes, which are exposed on the surface of human necrotic cells (), as new FHR5 ligands.
View Article and Find Full Text PDF