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Autophagic adaptations in diabetic cardiomyopathy differ between type 1 and type 2 diabetes.
https://asahi-u.repo.nii.ac.jp/records/6974
https://asahi-u.repo.nii.ac.jp/records/69747f393a49-2ee0-4b99-8ca5-8a3019a7c3ab
| Item type | 朝日大学 教育・研究業績(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-10-12 | |||||
| タイトル | ||||||
| タイトル | Autophagic adaptations in diabetic cardiomyopathy differ between type 1 and type 2 diabetes. | |||||
| 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 | Autophagy. | |||||
| 巻 | ||||||
| 値 | 11 | |||||
| 号 | ||||||
| 値 | 7 | |||||
| 掲載ページ | ||||||
| 値 | 1146-1160 | |||||
| 単著、共著の別 | ||||||
| 値 | 共著 | |||||
| 発行又は発表の年月 | ||||||
| 日付 | 2015-07-03 | |||||
| PubMed番号 | ||||||
| 値 | 26042865 | |||||
| 概要 | ||||||
| 値 | Little is known about the association between autophagy and diabetic cardiomyopathy. Also unknown are possible distinguishing features of cardiac autophagy in type 1 and type 2 diabetes. In hearts from streptozotocin-induced type 1 diabetic mice, diastolic function was impaired, though autophagic activity was significantly increased, as evidenced by increases in microtubule-associated protein 1 light chain 3/LC3 and LC3-II/-I ratios, SQSTM1/p62 (sequestosome 1) and CTSD (cathepsin D), and by the abundance of autophagic vacuoles and lysosomes detected electron-microscopically. AMP-activated protein kinase (AMPK) was activated and ATP content was reduced in type 1 diabetic hearts. Treatment with chloroquine, an autophagy inhibitor, worsened cardiac performance in type 1 diabetes. In addition, hearts from db/db type 2 diabetic model mice exhibited poorer diastolic function than control hearts from db/+ mice. However, levels of LC3-II, SQSTM1 and phosphorylated MTOR (mechanistic target of rapamycin) were increased, but CTSD was decreased and very few lysosomes were detected ultrastructurally, despite the abundance of autophagic vacuoles. AMPK activity was suppressed and ATP content was reduced in type 2 diabetic hearts. These findings suggest the autophagic process is suppressed at the final digestion step in type 2 diabetic hearts. Resveratrol, an autophagy enhancer, mitigated diastolic dysfunction, while chloroquine had the opposite effects in type 2 diabetic hearts. Autophagy in the heart is enhanced in type 1 diabetes, but is suppressed in type 2 diabetes. This difference provides important insight into the pathophysiology of diabetic cardiomyopathy, which is essential for the development of new treatment strategies. | |||||
