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気道平滑筋の遊走能と収縮能の制御に基づく喘息分子標的療法
https://kindai.repo.nii.ac.jp/records/18116
https://kindai.repo.nii.ac.jp/records/181161ac998b8-b60b-4c8f-9b5b-d34c086cab93
名前 / ファイル | ライセンス | アクション |
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25461201seika.pdf (190.5 kB)
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Item type | 研究報告書 / Research Paper(1) | |||||
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公開日 | 2016-10-14 | |||||
タイトル | ||||||
タイトル | 気道平滑筋の遊走能と収縮能の制御に基づく喘息分子標的療法 | |||||
タイトル | ||||||
言語 | en | |||||
タイトル | Molecularly-targeted therapy for asthma with a focus on migration and contractility of airway smooth muscle cells | |||||
著者 |
久米, 裕昭
× 久米, 裕昭 |
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言語 | ||||||
言語 | jpn | |||||
キーワード | ||||||
主題 | 喘息, phenotype change, 気道平滑筋, G protein, Ca2+ signaling, KCa channel, Rho-kinase, allosteric effect | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_18ws | |||||
資源タイプ | research report | |||||
著者(英) | ||||||
en | ||||||
KUME, Hiroaki | ||||||
著者 所属 | ||||||
近畿大学医学部; 准教授 | ||||||
著者所属(翻訳) | ||||||
Kindai University | ||||||
著者 役割 | ||||||
研究代表者 | ||||||
著者 外部リンク | ||||||
関連名称 | https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25461201/ | |||||
版 | ||||||
出版タイプ | NA | |||||
出版タイプResource | http://purl.org/coar/version/c_be7fb7dd8ff6fe43 | |||||
出版者 名前 | ||||||
出版者 | 近畿大学 | |||||
書誌情報 |
科学研究費助成事業研究成果報告書 (2015) p. 1-5, 発行日 2016 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | 研究成果の概要(和文):喘息の病態を気道平滑筋の表現型の変化として捉え、鍵となる蛋白を検索し、根元的な分子標的治療の確立を目的とした。その結果、病態の大部分は収縮性、増殖性の表現型の変化で生じ、それらの機序として、Ca2+-activated K+ channel/voltage-dependent Ca2+ channel の連関に由来する Ca2+ dynamics、および、RhoA/Rho-kinase 系を介する Ca2+ sensitization の関与を解明した。これらの Ca2+ signaling は、喘息治療のあらたな標的蛋白と考えられる。 研究成果の概要(英文):Alteration of contractility in airway smooth muscle (ASM) contributes to airflow limitation, airway hyperresponsiveness (AHR), and beta2-adrenergic desensitization. Alteration of synthesis contributes to airway remodeling via facilitation of the proliferation and migration in ASM. In our observation, Ca2+ dynamics through the large-conductance Ca2+-activated K+ channel/L-type voltage-dependent Ca2+ channel linkage, and Ca2+ sensitization through the RhoA/Rho-kinase pathway contribute not only to alterations in the contractile phenotype involved in airflow limitation, AHR and tolerance to beta2-adrenergic receptors, but also to alteration of the synthetic phenotype involved in airway remodeling. The Ca2+ signaling also contribute to the synergism (cross talk) in combination of beta2-adrenergic receptor agonists with muscarinic receptor antagonists. Therefore, the phenotype change in ASM via the Ca2+ signaling may be a novel target for development of asthmatic agents. |
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内容記述 | ||||||
内容記述タイプ | Other | |||||
内容記述 | 研究種目:基盤研究(C); 研究期間:2013~2015; 課題番号:25461201; 研究分野:医歯薬学; 科研費の分科・細目: | |||||
資源タイプ | ||||||
内容記述タイプ | Other | |||||
内容記述 | Research Paper | |||||
フォーマット | ||||||
内容記述タイプ | Other | |||||
内容記述 | application/pdf |