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Oxidative stress and chronic allograft nephropathy

Authors
 Hunjoo Ha  ;  Jehyun Park  ;  Hitoshi Endou  ;  Yu Seun Kim 
Citation
 YONSEI MEDICAL JOURNAL, Vol.45(6) : 1049-1052, 2004 
Journal Title
YONSEI MEDICAL JOURNAL
ISSN
 0513-5796 
Issue Date
2004
Keywords
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
Abstract
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 mycophenolic 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.
Files in This Item:
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Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Yu Seun(김유선) ORCID logo https://orcid.org/0000-0002-5105-1567
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/112972
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