{"created":"2023-07-27T06:51:39.991457+00:00","id":45176,"links":{},"metadata":{"_buckets":{"deposit":"dd0a8a33-cd45-4ae4-a5a4-d18f171fb016"},"_deposit":{"created_by":18,"id":"45176","owners":[18],"pid":{"revision_id":0,"type":"depid","value":"45176"},"status":"published"},"_oai":{"id":"oai:kanazawa-u.repo.nii.ac.jp:00045176","sets":["2812:2813:2816"]},"author_link":["21777","78623"],"item_9_biblio_info_8":{"attribute_name":"書誌情報","attribute_value_mlt":[{"bibliographicIssueDates":{"bibliographicIssueDate":"2018-09-07","bibliographicIssueDateType":"Issued"},"bibliographicPageStart":"5p.","bibliographicVolumeNumber":"2015-04-01 - 2018-03-31","bibliographic_titles":[{"bibliographic_title":"平成29(2017)年度 科学研究費補助金 基盤研究(C) 研究成果報告書"},{"bibliographic_title":"2017 Fiscal Year Final Research Report","bibliographic_titleLang":"en"}]}]},"item_9_creator_33":{"attribute_name":"著者別表示","attribute_type":"creator","attribute_value_mlt":[{"creatorNames":[{}],"nameIdentifiers":[{},{},{}]}]},"item_9_description_21":{"attribute_name":"抄録","attribute_value_mlt":[{"subitem_description":"肝臓から分泌されるヘパトカインであるセレノプロテインP (SeP)は、高血糖とインスリン抵抗性の病態形成に関与する。臨床的にインスリン抵抗性は、新規心不全発症の独立した危険因子だが、SePの心不全形成における役割は明らかでない。本研究では、心不全形成にかかわるSePの効果を検討するため、SePノックアウトマウス（KO）に横行大動脈縮窄モデルを作成した。SePKOは、WTと比較し、心不全死が有意に改善した。また、大動脈縮窄2週間後の左室重量、肺重量ならびに線維化の指標は、SePKOで有意に小さかった。これらの検討から、内因性のSePの欠損は圧負荷により誘導される心不全を抑制することが示唆された。","subitem_description_type":"Abstract"},{"subitem_description":"Selenoprotein P (SeP) is a liver-derived secretory protein that impairs insulin signal transduction and induces insulin resistance and hyperglycemia. Although clinical studies suggest the insulin resistance is an independent risk factor of heart failure, the role of SeP in pathogenesis of chronic heart failure is not well understood. We investigated the role of SeP in the regulation of cardiac remodeling in response to pressure overload. Transverse aortic constriction (TAC) was subjected to SeP knockout (KO) and wild-type (WT) mice for 2 weeks. The mortality rate following TAC was significantly decreased in SeP KO mice compared to WT mice. LV weight/body weight (BW) and Lung weight/BW were significantly smaller in SeP KO mice than in WT mice. Furthermore, mRNA expression of collagen 1a1 significantly less in SeP KO compared to WT. These results suggest that the absence of endogenous SeP attenuated cardiac hypertrophy, dysfunction and fibrosis in response to pressure overload in mice.","subitem_description_type":"Abstract"}]},"item_9_description_22":{"attribute_name":"内容記述","attribute_value_mlt":[{"subitem_description":"研究課題/領域番号:15K09135, 研究期間(年度):2015-04-01 - 2018-03-31","subitem_description_type":"Other"},{"subitem_description":"出典：研究課題「心不全状態での肝臓機能の破綻が心臓リモデリングへ与える影響御」課題番号15K09135\n（KAKEN：科学研究費助成事業データベース（国立情報学研究所）） \n（https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09135/15K09135seika/）を加工して作成","subitem_description_type":"Other"}]},"item_9_description_5":{"attribute_name":"提供者所属","attribute_value_mlt":[{"subitem_description":"金沢大学附属病院循環器内科","subitem_description_type":"Other"}]},"item_9_identifier_registration":{"attribute_name":"ID登録","attribute_value_mlt":[{"subitem_identifier_reg_text":"10.24517/00051515","subitem_identifier_reg_type":"JaLC"}]},"item_9_relation_28":{"attribute_name":"関連URI","attribute_value_mlt":[{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/search/?qm=50507043"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/search/?qm=50507043","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K09135/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-15K09135/","subitem_relation_type_select":"URI"}},{"subitem_relation_name":[{"subitem_relation_name_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09135/15K09135seika/"}],"subitem_relation_type_id":{"subitem_relation_type_id_text":"https://kaken.nii.ac.jp/report/KAKENHI-PROJECT-15K09135/15K09135seika/","subitem_relation_type_select":"URI"}}]},"item_9_version_type_25":{"attribute_name":"著者版フラグ","attribute_value_mlt":[{"subitem_version_resource":"http://purl.org/coar/version/c_ab4af688f83e57aa","subitem_version_type":"AM"}]},"item_files":{"attribute_name":"ファイル情報","attribute_type":"file","attribute_value_mlt":[{"accessrole":"open_date","date":[{"dateType":"Available","dateValue":"2019-04-18"}],"displaytype":"detail","filename":"HO-PR-USUI-S-kaken 2018-5p.pdf","filesize":[{"value":"366.9 kB"}],"format":"application/pdf","licensetype":"license_11","mimetype":"application/pdf","url":{"label":"HO-PR-USUI-S-kaken 2018-5p.pdf","url":"https://kanazawa-u.repo.nii.ac.jp/record/45176/files/HO-PR-USUI-S-kaken 2018-5p.pdf"},"version_id":"38fea344-ef8e-4020-a2bf-966acd10810f"}]},"item_language":{"attribute_name":"言語","attribute_value_mlt":[{"subitem_language":"jpn"}]},"item_resource_type":{"attribute_name":"資源タイプ","attribute_value_mlt":[{"resourcetype":"research report","resourceuri":"http://purl.org/coar/resource_type/c_18ws"}]},"item_title":"心不全状態での肝臓機能の破綻が心臓リモデリングへ与える影響","item_titles":{"attribute_name":"タイトル","attribute_value_mlt":[{"subitem_title":"心不全状態での肝臓機能の破綻が心臓リモデリングへ与える影響"},{"subitem_title":"Selenoprotein P, a liver-derived secretory protein, regulates pressure overload-induced cardiac remodeling","subitem_title_language":"en"}]},"item_type_id":"9","owner":"18","path":["2816"],"pubdate":{"attribute_name":"公開日","attribute_value":"2019-04-18"},"publish_date":"2019-04-18","publish_status":"0","recid":"45176","relation_version_is_last":true,"title":["心不全状態での肝臓機能の破綻が心臓リモデリングへ与える影響"],"weko_creator_id":"18","weko_shared_id":-1},"updated":"2023-07-27T13:00:46.708968+00:00"}