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Nox-2 is a modulator of fibrogenesis in kidney allografts

A Djamali1, A Vidyasagar, M Adulla

  • 1Nephrology Section, Department of Medicine, University of Wisconsin Madison School of Medicine and Public Health, Madison, WI, USA. axd@medicine.wisc.edu

American Journal of Transplantation : Official Journal of the American Society of Transplantation and the American Society of Transplant Surgeons
|November 4, 2008
PubMed

Insights

The study reveals that NADPH oxidase 2 (Nox-2) drives kidney allograft tubulointerstitial fibrosis by promoting oxidative stress and epithelial-to-mesenchymal transition (EMT). Inhibiting Nox-2 reduces fibrosis markers and improves graft health.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Kidney allograft tubulointerstitial fibrosis is a major cause of graft loss.
  • The role of NADPH oxidase (Nox) enzymes in this process remains incompletely understood.

Purpose of the Study:

  • To investigate the role of classical phagocytic NADPH oxidase (Nox) in kidney allograft tubulointerstitial fibrosis.
  • To elucidate the specific Nox isoforms and cellular sources involved in fibrosis development.

Main Methods:

  • Immunofluorescence staining for Nox-2, p22phox, alpha-SMA, and other markers in human and rat kidney allografts.
  • In vitro studies using NRK52E cells treated with Cyclosporine A, TGF-beta1, and angiotensin II.
  • Treatment of allografts with Nox inhibitors (DPI, apocynin) and assessment of fibrosis markers.

Main Results:

  • Nox-2 and p22phox colocalized in fibrotic areas of human and rat kidney allografts.
  • Nox-2 expression was elevated in interstitial macrophages and myofibroblasts, correlating with oxidative stress and fibrogenesis markers.
  • Nox inhibition reduced fibrosis markers (fibronectin, phospho-Smad2) and promoted epithelial markers (E-cadherin).
  • Pro-fibrotic stimuli increased Nox-2 mRNA, which was reversed by Nox inhibitors.

Conclusions:

  • Nox-2 plays a significant role in the pathogenesis of kidney allograft tubulointerstitial fibrosis.
  • Nox-2 contributes to fibrosis through activation of Smad2, promotion of epithelial-to-mesenchymal transition (EMT), and myofibroblast activation.
  • Targeting Nox-2 may represent a therapeutic strategy to mitigate kidney allograft fibrosis.

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