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A dipeptidyl peptidase-4 inhibitor ameliorates hypertensive cardiac remodeling via angiotensin-II/sodium-proton pump exchanger-1 axis
http://hdl.handle.net/2237/25205
http://hdl.handle.net/2237/252053a078e30-13ab-4e44-82eb-67f1f8495b9b
名前 / ファイル | ライセンス | アクション |
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Final-20160626-HK-Manuscript-Main.pdf ファイル公開:2017/09/01 (317.2 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2016-12-15 | |||||
タイトル | ||||||
タイトル | A dipeptidyl peptidase-4 inhibitor ameliorates hypertensive cardiac remodeling via angiotensin-II/sodium-proton pump exchanger-1 axis | |||||
言語 | en | |||||
著者 |
Kawase, Haruya
× Kawase, Haruya× Bando, K. Yasuko× Nishimura, Kazuyuki× Aoyama, Morihiko× Monji, Akio× Murohara, Toyoaki |
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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 | |||||
権利 | ||||||
言語 | en | |||||
権利情報 | © 2016. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ | |||||
抄録 | ||||||
内容記述 | Background: To address the impact of antidiabetic drugs on cardiovascular safety is a matter of clinical concern. Preclinical studies revealed that various protective effects of dipeptidyl peptidase-4 inhibitor (DPP4i) on cardiovascular disease; however, its impact of on hypertension remains controversial. Methods and results: Teneligliptin (TEN; 10 mg/kg/day/p.o.) ameliorates hypertension and cardiac remodeling by normalizing a rise of angiotensin-II (AngII) that specifically observed in spontaneously hypertensive rats (SHR). TEN had no effects on vasculature and concentrations of the DPP4-related vasoactive peptides (bradykinin, neuropeptide Y, and atrial natriuretic peptide). The primary action of TEN on BP lowering was due to restoring the AngII-induced manifestation of congestive heart failure observed in SHR. Sodium-proton pump exchanger type 1 (NHE-1) is a regulator of intracellular acidity (pHi) and implicated pathophysiological role in cardiac remodeling occurred in diseased myocardium. Cardiac NHE-1 expression level was increased in SHR and this was restored in TEN-treated SHR. AngII directly augmented cardiac NHE-1 expression and its activity that contributed to hypertrophic response. TEN attenuated the AngII-induced cardiac hypertrophy with decline in pHi via suppression of NHE-1. Loss of NHE-1 activity by specific inhibitor or RNA silencing promoted intracellular acidification and consistently attenuated the AngII-mediated cardiac hypertrophy. Conclusion: The present study revealed the protective actions of TEN on hypertension and comorbid cardiac remodeling via AngII/NHE-1 axis and the novel pathophysiological roles of intracellular acidification via NHE-1 in cardiac hypertrophy. | |||||
言語 | en | |||||
内容記述タイプ | Abstract | |||||
出版者 | ||||||
言語 | en | |||||
出版者 | Elsevier | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプresource | http://purl.org/coar/resource_type/c_6501 | |||||
タイプ | journal article | |||||
出版タイプ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | https://doi.org/10.1016/j.yjmcc.2016.06.066 | |||||
ISSN | ||||||
収録物識別子タイプ | PISSN | |||||
収録物識別子 | 0022-2828 | |||||
書誌情報 |
en : Journal of Molecular and Cellular Cardiology 巻 98, p. 37-47, 発行日 2016-09 |
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著者版フラグ | ||||||
値 | author | |||||
URI | ||||||
識別子 | http://doi.org/10.1016/j.yjmcc.2016.06.066 | |||||
識別子タイプ | DOI | |||||
URI | ||||||
識別子 | http://hdl.handle.net/2237/25205 | |||||
識別子タイプ | HDL |