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Factor H-related protein 1 (FHR-1): A complement regulatory protein and guardian of necrotic type surfaces.

Authors
  • Skerka, Christine1
  • Pradel, Gabriele2
  • Halder, Luke D1
  • Zipfel, Peter F1
  • Zipfel, Svante L H3
  • Strauß, Olaf4
  • 1 Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, Beutenbergstr. 11a, 07745, Jena, Germany. , (Germany)
  • 2 Division of Cellular and Applied Infection Biology, RWTH Aachen University, 52074, Aachen, Germany. , (Germany)
  • 3 Clinic for Heart and Visceral Surgery, Center of Heart Diseases, University Hospital Hamburg-Eppendorf, 20251, Hamburg, Germany. , (Germany)
  • 4 Experimental Ophtalmology, Charité University Medicine, Campus Virchow Clinic, Augustusplatz 1, 13353, Berlin, Germany. , (Germany)
Type
Published Article
Journal
British Journal of Pharmacology
Publisher
Wiley (Blackwell Publishing)
Publication Date
Oct 21, 2020
Identifiers
DOI: 10.1111/bph.15290
PMID: 33085794
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Factor H-related protein 1 (FHR-1) is a member of the factor H protein family, which is involved in regulating innate immune complement reactions. Genetic modification of the encoding gene, CFHR1 on human chromosome 1, is involved in diseases such as age-related macular degeneration, C3-glomerulopathy, and atypical hemolytic uremic syndrome, indicating an important role for FHR-1 in human health. Recent research data demonstrate that FHR-1 levels increase in IgA nephropathy and ANCA vasculitis and that FHR-1 induces strong inflammation in monocytes on necrotic-type surfaces, suggesting a complement-independent role. These new results increase our knowledge about the role of this complement protein in pathology and provide a new therapeutic target, particularly in the context of inflammatory diseases induced by necrosis. This review summarizes current knowledge about FHR-1 and discusses its role in complement reactions and inflammation. This article is protected by copyright. All rights reserved.

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