Oxidative stress and chronic allograft nephropathy

Hunjoo Ha, Jehyun Park, Yu Seun Kim, Hitoshi Endou

Research output: Contribution to journalReview articlepeer-review

33 Scopus citations


Oxidative stress defined as outbalanced generation of reactive oxygen species (ROS) than the existing antioxidative defense mechanisms plays an important role in tissue injury. Ischemia/reperfusion accompanied during organ transplantation is well- established oxidative stress-induced tissue injury. We hypothesized that oxidative stress may also play a role in the development and progression of chronic allograft nephropathy (CAN), since that ROS are major signaling molecules of growth factors and cytokines [platelet-derived growth factors, transforming growth factor-β1 (TGF-β1)] upregulated in the Kidney of CAN, that ROS in turn upregulate TGF-β1, and that myeophenolic acid may inhibit features of CAN [proliferation and extracellular matrix (ECM) accumulation in vascular smooth muscle cells and glomerular mesangial cells] through inhibiting cellular ROS. Cellular ROS activate signal transduction cascade (protein kinase C, mitogen-activated protein kinases, and janus kinases) and transcription factors (nuclear factor-κB, activated protein-1, specificity protein 1, and signal transducers and activators of transcription) leading to regulation of genes and proteins involved in cellular proliferation, ECM remodeling, and apoptosis accompanied in CAN. This review is intended to provide an overview of oxidative stress in renal allograft nephropathy.

Original languageEnglish
Pages (from-to)1049-1052
Number of pages4
JournalYonsei Medical Journal
Issue number6
StatePublished - 31 Dec 2004


  • Antioxidants
  • Chronic allograft nephropathy
  • Ischemia-reperfusion injury
  • Nicotinamide adenosine dinucleotide phosphate (reduced form) oxidase
  • Platelet-derived growth factor
  • Reactive oxygen species
  • Transforming growth factor-β1


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