| Item type |
学術雑誌論文 / Journal Article(1) |
| 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
Kadowaki, Ayumi
Suzuki, Takashi
Ito, Hiroshi
Watanabe, Hiroyuki
Imai, Yumiko
Kuba, Keiji
|
| 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
|
| 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/). |
iA_2022_63.pdf (2.7 MB)
