WEKO3
インデックスリンク
アイテム
Restriction of food intake prevents postinfarction heart failure by enhancing autophagy in the surviving cardiomyocytes.
https://asahi-u.repo.nii.ac.jp/records/3233
https://asahi-u.repo.nii.ac.jp/records/323377cf31bb-3052-42ab-907f-8643a2542ab7
| Item type | 朝日大学 教育・研究業績(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2015-02-25 | |||||
| タイトル | ||||||
| タイトル | Restriction of food intake prevents postinfarction heart failure by enhancing autophagy in the surviving cardiomyocytes. | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_1843 | |||||
| 資源タイプ | other | |||||
| アクセス権 | ||||||
| アクセス権 | metadata only access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
| 業績分類 | ||||||
| 値 | 学術雑誌論文 | |||||
| 教員氏名 |
竹村, 元三
× 竹村, 元三 |
|||||
| 発行、発表雑誌等、又は発表学会等の名称 | ||||||
| 値 | Am J Pathol. | |||||
| 巻 | ||||||
| 値 | 184 | |||||
| 号 | ||||||
| 値 | 5 | |||||
| 掲載ページ | ||||||
| 値 | 1384-1394 | |||||
| 単著、共著の別 | ||||||
| 値 | 共著 | |||||
| 発行又は発表の年月 | ||||||
| 日付 | 2014-05 | |||||
| PubMed番号 | ||||||
| 値 | 24641899 | |||||
| 概要 | ||||||
| 値 | We investigated the effect of restriction of food intake, a potent inducer of autophagy, on postinfarction cardiac remodeling and dysfunction. Myocardial infarction was induced in mice by left coronary artery ligation. At 1 week after infarction, mice were randomly divided into four groups: the control group was fed ad libitum (100%); the food restriction (FR) groups were fed 80%, 60%, or 40% of the mean amount of food consumed by the control mice. After 2 weeks on the respective diets, left ventricular dilatation and hypofunction were apparent in the control group, but both parameters were significantly mitigated in the FR groups, with the 60% FR group showing the strongest therapeutic effect. Cardiomyocyte autophagy was strongly activated in the FR groups, as indicated by up-regulation of microtubule-associated protein 1 light chain 3-II, autophagosome formation, and myocardial ATP content. Chloroquine, an autophagy inhibitor, completely canceled the therapeutic effect of FR. This negative effect was associated with reduced activation of AMP-activated protein kinase and of ULK1 (a homolog of yeast Atg1), both of which were enhanced in hearts from the FR group. In vitro, the AMP-activated protein kinase inhibitor compound C suppressed glucose depletion-induced autophagy in cardiomyocytes, but did not influence activity of chloroquine. Our findings imply that a dietary protocol with FR could be a preventive strategy against postinfarction heart failure. | |||||
