The Role of Nuclear Factor κB Activation in the Development of Renal Fibrosis
-
- 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
この論文をさがす
抄録
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>
収録刊行物
-
- Journal of Pharmacological Sciences
-
Journal of Pharmacological Sciences 100 (1), 17-21, 2006
公益社団法人 日本薬理学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390001205175323392
-
- NII論文ID
- 10018240945
-
- NII書誌ID
- AA11806667
-
- ISSN
- 13478648
- 13478613
-
- NDL書誌ID
- 7782929
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可