Evaluation of cancer-derived myocardial impairments using a mouse model.

• Material Type: 博士論文
• Title: Evaluation of cancer-derived myocardial impairments using a mouse model.
• Author/Editor: Miyagawa, Yoshihiro; Nukaga, Shota; Mori, Takuya; Fujiwara-Tani, Rina; Fujii, Kiyomu; Mori, Shiori; Goto, Kei; Kishi, Shingo; Sasaki, Takamitsu; Nakashima, Chie; Ohmori, Hitoshi; Kawahara, Isao; Luo, Yi; Kuniyasu, Hiroki
• Author Heading: Miyagawa, Yoshihiro; Nukaga, Shota; Mori, Takuya; Fujiwara-Tani, Rina; Fujii, Kiyomu; Mori, Shiori; Goto, Kei; Kishi, Shingo; Sasaki, Takamitsu; Nakashima, Chie; Ohmori, Hitoshi; Kawahara, Isao; Luo, Yi; Kuniyasu, Hiroki
• Publication, Distribution, etc.: Impact Journals
• Publication Date: 2020-10-13
• Publication Date (W3CDTF): 2020-10-13
• Alternative Title: マウスモデルを用いたがん性心筋障害の評価
• Periodical title: Oncotarget
• No. or year of volume/issue: 11 41
• Volume: 11
• Issue: 41
• Pages: 3712-3722
• ISSN (Periodical Title): ISSN : 1949-2553
• Degree grantor/type: 奈良県立医科大学
• Date Granted: 2022-03-15
• Dissertation Number: 甲第820号
• Degree Type: 博士（医学）
• Text Language Code: eng
• Subject Heading: cachexia; myocardium; atrophy; mitochondria; oxidative stress
• Target Audience: 一般
• Note (General): type:Thesis; Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.; 博士（医学）・甲第820号・令和4年3月15日; Copyright: © 2020 Miyagawa et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0 https://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.; identifier:Oncotarget Vol.11 No.41 p.3712-3722 (2020 Oct); identifier:19492553; identifier:http://ginmu.naramed-u.ac.jp/dspace/handle/10564/4003; identifier:Oncotarget, 11(41): 3712-3722
• Access Restrictions: インターネット公開
• Related Material (DOI): 10.18632/oncotarget.27759
• 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/10564/4003/1/01%e7%94%b2820%e6%9c%ac%e6%96%87%e3%81%ae%e8%a6%81%e6%97%a8.pdf fulltext

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