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Involvement of bone-marrow-derived cells in kidney fibrosis
http://hdl.handle.net/2297/26306
http://hdl.handle.net/2297/26306338e6985-0c86-4a0e-8db1-77b9108a4e23
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
ME-PR-FURUICHI-K-8.pdf (62.6 kB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-10-03 | |||||
| タイトル | ||||||
| タイトル | Involvement of bone-marrow-derived cells in kidney fibrosis | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| 著者 |
Wada, Takashi
× Wada, Takashi× Sakai, Norihiko× Sakai, Yoshio× Matsushima, Kouji× Kaneko, Shuichi× Furuichi, Kengo |
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| 提供者所属 | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | 金沢大学医薬保健研究域医学系 | |||||
| 書誌情報 |
Clinical and Experimental Nephrology 巻 15, 号 1, p. 8-13, 発行日 2011-02-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1342-1751 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AA11126935 | |||||
| DOI | ||||||
| 関連タイプ | isVersionOf | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1007/s10157-010-0372-2 | |||||
| 出版者 | ||||||
| 出版者 | Japanese Society of Nephrology / Springer Verlag (Germany) | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Cellular mechanisms have been proposed in the pathogenesis of fibrotic processes in the kidney. In this setting, cell sources underlying the generation of matrix-producing cells in diseased kidneys have been categorized as activated resident stromal cells (e.g., fibroblasts, pericytes), infiltrating bone-marrow-derived cells (e.g., fibrocytes, T cells, macrophages), and cells derived from epithelial-mesenchymal transition/endothelial-mesenchymal transition. Among these cell sources, accumulating evidence has shed light on the involvement of bone-marrow-derived cells, including monocytes/macrophages, and a circulating mesenchymal progenitor cell, fibrocyte, in the progression of fibrosis in kidney. Bone-marrow-derived cells positive for CD45 or CD34, and type 1 (pro)collagen dependent on the chemokine and renin-angiotensin systems migrate into diseased kidneys and enhance synthesis matrix protein, cytokines/chemokines, and profibrotic growth factors, which may promote and escalate chronic inflammatory processes and possible interaction with resident stromal cells, thereby perpetuating kidney fibrosis. © 2010 Japanese Society of Nephrology. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | AM | |||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
