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ADAMTS7-Mediated Complement Factor H Degradation Potentiates Complement Activation to Contributing to Renal Injuries.

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Extracellular protease ADAMTS7 degrades complement factor H (CFH), worsening kidney injury. Targeting ADAMTS7 may treat complement-mediated renal diseases without increasing infection risk.

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Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Complement factor H (CFH) dysfunction is linked to renal injuries.
  • Mechanisms of CFH dysfunction in kidney disease are not fully understood.

Purpose of the Study:

  • Investigate extracellular protease-mediated degradation as a cause of CFH dysfunction.
  • Explore the role of ADAMTS7 in complement-mediated renal injuries.

Main Methods:

  • Identified CFH-binding proteases in lupus mouse kidneys using interactome analysis.
  • Performed in vitro cleavage assays to confirm CFH degradation by ADAMTS7.
  • Utilized lupus nephritis and renal ischemia-reperfusion (I/R) injury models in wild-type and ADAMTS7 knockout mice.

Main Results:

  • ADAMTS7 was identified as a CFH-binding protease that degrades CFH.
  • ADAMTS7 upregulation correlated with CFH reduction in lupus models and patients.
  • ADAMTS7 deficiency protected against renal injury by reducing complement activation, without impairing bacterial defense.
  • CFH silencing reversed the protective effects of ADAMTS7 deficiency.

Conclusions:

  • ADAMTS7-mediated CFH degradation drives complement activation and renal injury.
  • ADAMTS7 represents a potential therapeutic target for anticomplement therapy with a low risk of infection.