The Role of Nuclear Factor κB Activation in the Development of Renal Fibrosis

DOI Web Site 被引用文献6件 参考文献30件
  • Tamada Satoshi
    Department of Urology, Osaka City University Medical School, Japan
  • Asai Toshihiro
    Department of Urology, Osaka City University Medical School, Japan
  • Kuwabara Nobuyuki
    Department of Urology, Osaka City University Medical School, Japan
  • Iwai Tomoaki
    Department of Urology, Osaka City University Medical School, Japan
  • Uchida Junji
    Department of Urology, Osaka City University Medical School, Japan
  • Teramoto Kae
    Department of Applied Pharmacology and Therapeutics, Osaka City University Medical School, Japan
  • Kaneda Noriko
    Department of Applied Pharmacology and Therapeutics, Osaka City University Medical School, Japan
  • Yukimura Tokihito
    Department of Applied Pharmacology and Therapeutics, Osaka City University Medical School, Japan
  • Komiya Toshiyuki
    Department of Medicine, The Tazuke Kofukai, Medical Research Institute, Kitano Hospital, Japan
  • Nakatani Tatsuya
    Department of Urology, Osaka City University Medical School, Japan
  • Miura Katsuyuki
    Department of Applied Pharmacology and Therapeutics, Osaka City University Medical School, Japan

書誌事項

タイトル別名
  • Molecular Mechanisms and Therapeutic Strategies of Chronic Renal Injury: The Role of Nuclear Factor .KAPPA.B Activation in the Development of Renal Fibrosis
  • Role of Nuclear Factor カッパ B Activation in the Development of Renal Fibrosis
  • Molecular Mechanisms and Therapeutic Strategies of Chronic Renal Injury: The Role of Nuclear Factor κB Activation in the Development of Renal Fibrosis

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Tubulointerstitial fibrosis is a common feature of many progressive renal diseases and is a main determinant that leads to an irreversible loss of renal function. In chronic cyclosporin A nephrotoxicity, we previously reported that inflammatory responses such as macrophage infiltration preceded interstitial fibrosis. This inflammation was accompanied by an elevation in renal nuclear factor κB (NF-κB) activity. Similar findings were obtained in chronic tacrolimus nephrotoxicity and obstructive nephropathy. Inhibition of NF-κB markedly attenuated renal inflammation and interstitial fibrosis in these models. Furthermore, administration of oral adsorbent (Kremezin®) significantly attenuated the increase in renal NF-κB activity and concomitantly reduced interstitial inflammation and renal fibrosis in chronic renal failure rats. Elimination of indoxyl sulfate by this adsorbent is likely involved in this mechanism since it is known that indoxyl sulfate activates NF-κB in renal tubular cells. It is suggested that strategy aiming at NF-κB inhibition is important to prevent the progression of renal fibrosis.<br>

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