Suppressed soluble Fms-like tyrosine kinase-1 production aggravates atherosclerosis in chronic kidney disease.

• 資料種別: 博士論文
• タイトル: Suppressed soluble Fms-like tyrosine kinase-1 production aggravates atherosclerosis in chronic kidney disease.
• 著者・編者: Matsui, Masaru; Takeda, Yukiji; Uemura, Shiro; Matsumoto, Takaki; Seno, Ayako; Onoue, Kenji; Tsushima, Hideo; Morimoto, Katsuhiko; Soeda, Tsunenari; Okayama, Satoshi; Somekawa, Satoshi; Samejima, Ken-ichi; Kawata, Hiroyuki; Kawakami, Rika; Nakatani, Kimihiko; Iwano, Masayuki; Saito, Yoshihiko
• 著者標目: Matsui, Masaru; Takeda, Yukiji; Uemura, Shiro; Matsumoto, Takaki; Seno, Ayako; Onoue, Kenji; Tsushima, Hideo; Morimoto, Katsuhiko; Soeda, Tsunenari; Okayama, Satoshi; Somekawa, Satoshi; Samejima, Ken-ichi; Kawata, Hiroyuki; Kawakami, Rika; Nakatani, Kimihiko; Iwano, Masayuki; Saito, Yoshihiko
• 出版事項: Nature Publishing
• 出版年月日等: 2014-02
• 出版年（W3CDTF）: 2014-02
• 並列タイトル等: 慢性腎臓病では血中可溶型fms様チロシンキナーゼ-1産生の減少が動脈硬化症を悪化させる
• タイトル（掲載誌）: Kidney international
• 巻号年月日等（掲載誌）: 85 2
• 掲載巻: 85
• 掲載号: 2
• 掲載ページ: 393-403
• ISSN（掲載誌）: ISSN : 0085-2538
• 授与機関名: 奈良県立医科大学
• 授与年月日: 2014-03-17
• 報告番号: 甲第614号
• 学位: 博士（医学）
• 本文の言語コード: eng
• 件名標目: atherosclerosis; chronic kidney disease; placental growth factor; soluble fms-like; tyrosine kinase-1
• 対象利用者: 一般
• 一般注記: type:Thesis; Patients with chronic kidney disease (CKD) die of cardiovascular diseases for unknown reasons. Blood vessel formation in plaques and its relationship with plaque stability could be involved with signaling through the Flt-1 receptor and its ligands, vascular endothelial growth factor, and the closely related placental growth factor (PlGF). Flt-1 also exists as a circulating regulatory splice variant short-inhibitory form (sFlt-1) that serves as a decoy receptor, thereby inactivating PlGF. Heparin releases sFlt-1 by displacing the sFlt-1 heparin-binding site from heparin sulfate proteoglycans. Heparin could provide diagnostic inference or could also induce an antiangiogenic state. In the present study, postheparin sFlt-1 levels were lower in CKD patients than in control subjects. More importantly, sFlt-1 levels were inversely related to atherosclerosis in CKD patients, and this correlation was more robust after heparin injection, as verified by subsequent cardiovascular events. Knockout of apolipoprotein E (ApoE) and/or sFlt-1 showed that the absence of sFlt-1 worsened atherogenesis in ApoE-deficient mice. Thus, the relationship between atherosclerosis and PlGF signaling, as regulated by sFlt-1, underscores the underappreciated role of heparin in sFlt-1 release. These clinical and experimental data suggest that novel avenues into CKD-dependent atherosclerosis and its detection are warranted.; 博士（医学）・甲614号・平成26年3月17日; identifier:Kidney international Vol.85 No.2 p.393-403; identifier:00852538; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/2699; identifier:Kidney international, 85(2): 393-403
• オンライン閲覧公開範囲: インターネット公開
• 関連情報（DOI）: 10.1038/ki.2013.339
• 連携機関・データベース: 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）; https://irdb.nii.ac.jp
• 提供元機関・データベース: 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

目次

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2699/1/01%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2699/2/02%e5%af%a9%e6%9f%bb%e8%a6%81%e6%97%a8.pdf fulltext

http://ginmu.naramed-u.ac.jp/dspace/bitstream/10564/2699/6/03%e6%9c%ac%e6%96%87.pdf fulltext