HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Terminal complement effectors in atypical hemolytic uremic syndrome: C5a, C5b-9, or a bit of both?

Abstract
The role of the terminal complement pathway as the cause of atypical hemolytic uremic syndrome (aHUS) is widely recognized, but the relative contribution of the effectors C5a/C5aR1 and C5b-9 to disease pathogenesis has not been defined. Using FHR/R mice carrying a factor H mutation that causes cell surface complement alternative pathway dysregulation, Ueda documented that in FHR/R mice, C5b-9 causes renal thrombotic microangiopathy (TMA) whereas C5a/C5aR drives macrovascular thrombosis. This commentary addresses the implications and limitations of this study.
AuthorsMarina Noris, Giuseppe Remuzzi
JournalKidney international (Kidney Int) Vol. 96 Issue 1 Pg. 13-15 (07 2019) ISSN: 1523-1755 [Electronic] United States
PMID31229026 (Publication Type: Journal Article, Comment)
CopyrightCopyright © 2019 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.
Chemical References
  • Complement Membrane Attack Complex
  • Complement Factor H
Topics
  • Animals
  • Atypical Hemolytic Uremic Syndrome
  • Complement Factor H (genetics)
  • Complement Membrane Attack Complex
  • Mice
  • Mutation
  • Thrombosis

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: