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

• Material Type: 博士論文
• Title: Suppressed soluble Fms-like tyrosine kinase-1 production aggravates atherosclerosis in chronic kidney disease.
• Author/Editor: 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
• Author Heading: 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
• Publication, Distribution, etc.: Nature Publishing
• Publication Date: 2014-02
• Publication Date (W3CDTF): 2014-02
• Alternative Title: 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
• Periodical title: Kidney international
• No. or year of volume/issue: 85 2
• Volume: 85
• Issue: 2
• Pages: 393-403
• ISSN (Periodical Title): ISSN : 0085-2538
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2014-03-17
• Dissertation Number: 甲第614号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: atherosclerosis; chronic kidney disease; placental growth factor; soluble fms-like; tyrosine kinase-1
• Target Audience: 一般
• Note (General): 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
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.1038/ki.2013.339
• Data Provider (Database): 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
• Original Data Provider (Database): 奈良県立医科大学 : 奈良県立医科大学機関リポジトリ GINMU

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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