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Loss of Apelin Augments Angiotensin II-Induced Cardiac Dysfunction and Pathological Remodeling
http://hdl.handle.net/10295/00006206
http://hdl.handle.net/10295/000062067ee52a1c-a6f3-4665-9449-897bd9d63bc0
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
iA_2022_63.pdf (2.7 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2023-02-23 | |||||
| タイトル | ||||||
| タイトル | Loss of Apelin Augments Angiotensin II-Induced Cardiac Dysfunction and Pathological Remodeling | |||||
| 言語 | en | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | apelin | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | APJ receptor | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | angiotensin II | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | angiotensin-converting enzyme 2 | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | ACE inhibitor | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | transforming growth-factor beta | |||||
| 主題 | ||||||
| 主題Scheme | Other | |||||
| 主題 | heart failure | |||||
| 資源タイプ | ||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
| 資源タイプ | journal article | |||||
| アクセス権 | ||||||
| アクセス権 | open access | |||||
| アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
| 作成者 |
Sato, Teruki
× Sato, Teruki× Kadowaki, Ayumi× Suzuki, Takashi× Ito, Hiroshi× Watanabe, Hiroyuki× Imai, Yumiko× Kuba, Keiji |
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| 内容記述 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Apelin is an inotropic and cardioprotective peptide that exhibits beneficial effects through activation of the APJ receptor in the pathology of cardiovascular diseases. Apelin induces the expression of angiotensin-converting enzyme 2 (ACE2) in failing hearts, thereby improving heart function in an angiotensin 1-7-dependent manner. Whether apelin antagonizes the over-activation of the renin-angiotensin system in the heart remains elusive. In this study we show that the detrimental effects of angiotensin II (Ang II) were exacerbated in the hearts of aged apelin-gene-deficient mice. Ang II-mediated cardiac dysfunction and hypertrophy were augmented in apelin knockout mice. The loss of apelin increased the ratio of angiotensin-converting enzyme (ACE) to ACE2 expression in the Ang II-stressed hearts, and Ang II-induced cardiac fibrosis was markedly enhanced in apelin knockout mice. mRNA expression of pro-fibrotic genes, such as transforming growth-factor beta (TGF-beta) signaling, were significantly upregulated in apelin knockout hearts. Consistently, treatment with the ACE-inhibitor Captopril decreased cardiac contractility in apelin knockout mice. In vitro, apelin ameliorated Ang II-induced TGF-beta expression in primary cardiomyocytes, accompanied with reduced hypertrophy. These results provide direct evidence that endogenous apelin plays a crucial role in suppressing Ang II-induced cardiac dysfunction and pathological remodeling. | |||||
| 言語 | en | |||||
| 出版タイプ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
| 書誌情報 |
en : INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 巻 20, 号 2, 発行日 2019 |
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| 収録物識別子 | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1422-0067 | |||||
| 出版者 | ||||||
| 出版者 | MDPI | |||||
| 関連情報 | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.3390/ijms20020239 | |||||
| 権利情報 | ||||||
| 権利情報 | © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
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