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The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction

Myocardial remodeling serves an important role in the pathophysiology of coronary heart disease. The angiotensin-converting enzyme (ACE)2-angiotensin-(1–7) [Ang (1–7)]-Mas receptor (MasR) axis is a key regulator in myocardial remodeling and development of heart failure. To investigate how ACE2-Ang-(...

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Autores principales: Wang, Juan, He, Wen, Guo, Liping, Zhang, Yin, Li, Hui, Han, Suxia, Shen, Difei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5561970/
https://www.ncbi.nlm.nih.gov/pubmed/28656296
http://dx.doi.org/10.3892/mmr.2017.6848
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author Wang, Juan
He, Wen
Guo, Liping
Zhang, Yin
Li, Hui
Han, Suxia
Shen, Difei
author_facet Wang, Juan
He, Wen
Guo, Liping
Zhang, Yin
Li, Hui
Han, Suxia
Shen, Difei
author_sort Wang, Juan
collection PubMed
description Myocardial remodeling serves an important role in the pathophysiology of coronary heart disease. The angiotensin-converting enzyme (ACE)2-angiotensin-(1–7) [Ang (1–7)]-Mas receptor (MasR) axis is a key regulator in myocardial remodeling and development of heart failure. To investigate how ACE2-Ang-(1–7)-MasR axis function on myocardial remodeling and cardiac fibrosis in post-myocardial infarction (MI), male Sprague-Dawley rats (weight, 200±20 g) were used to establish the model of myocardial infarction by ligating the left coronary artery. The present study suggests that telmisartan (Tel) and olmesartan (Olm) (5 mg/kg/d) can inhibit myocardial remodeling of post-myocardial infarction through the ACE2-Ang (1–7)-MasR pathway. Administration of Tel or Olm was demonstrated to significantly inhibit collagen deposition using Masson staining. In addition, telmisartan and olmesartan was indicated to antagonize angiotensin II (Ang II) and upregulate ACE2, MasR, Ang (1–7) expression in myocardial tissue using immunoassay and ELISA test, and the effect of Olm was more marked than that of Tel at the same dosage. Simultaneously, compared with the MI or Sham group, the mRNA and protein expression of ACE2, Ang II and MasR in myocardial tissue demonstrated a remarkable increase in the Olm group, when compared with the Tel group. Taken together, our data demonstrated that ACE2-Ang (1–7)-MasR axis may present a potential protective role in the development of myocardial remodeling and may provide a new target for drug development of cardiac fibrosis. In conclusion, Olm is superior to Tel in inhibiting myocardial local Ang II level reducing myocardial collagen deposition and improving myocardial remodeling by upregulating the expression of ACE2, Ang (1–7) and MasR.
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spelling pubmed-55619702017-10-23 The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction Wang, Juan He, Wen Guo, Liping Zhang, Yin Li, Hui Han, Suxia Shen, Difei Mol Med Rep Articles Myocardial remodeling serves an important role in the pathophysiology of coronary heart disease. The angiotensin-converting enzyme (ACE)2-angiotensin-(1–7) [Ang (1–7)]-Mas receptor (MasR) axis is a key regulator in myocardial remodeling and development of heart failure. To investigate how ACE2-Ang-(1–7)-MasR axis function on myocardial remodeling and cardiac fibrosis in post-myocardial infarction (MI), male Sprague-Dawley rats (weight, 200±20 g) were used to establish the model of myocardial infarction by ligating the left coronary artery. The present study suggests that telmisartan (Tel) and olmesartan (Olm) (5 mg/kg/d) can inhibit myocardial remodeling of post-myocardial infarction through the ACE2-Ang (1–7)-MasR pathway. Administration of Tel or Olm was demonstrated to significantly inhibit collagen deposition using Masson staining. In addition, telmisartan and olmesartan was indicated to antagonize angiotensin II (Ang II) and upregulate ACE2, MasR, Ang (1–7) expression in myocardial tissue using immunoassay and ELISA test, and the effect of Olm was more marked than that of Tel at the same dosage. Simultaneously, compared with the MI or Sham group, the mRNA and protein expression of ACE2, Ang II and MasR in myocardial tissue demonstrated a remarkable increase in the Olm group, when compared with the Tel group. Taken together, our data demonstrated that ACE2-Ang (1–7)-MasR axis may present a potential protective role in the development of myocardial remodeling and may provide a new target for drug development of cardiac fibrosis. In conclusion, Olm is superior to Tel in inhibiting myocardial local Ang II level reducing myocardial collagen deposition and improving myocardial remodeling by upregulating the expression of ACE2, Ang (1–7) and MasR. D.A. Spandidos 2017-08 2017-06-23 /pmc/articles/PMC5561970/ /pubmed/28656296 http://dx.doi.org/10.3892/mmr.2017.6848 Text en Copyright: © Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Wang, Juan
He, Wen
Guo, Liping
Zhang, Yin
Li, Hui
Han, Suxia
Shen, Difei
The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title_full The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title_fullStr The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title_full_unstemmed The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title_short The ACE2-Ang (1–7)-Mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
title_sort ace2-ang (1–7)-mas receptor axis attenuates cardiac remodeling and fibrosis in post-myocardial infarction
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5561970/
https://www.ncbi.nlm.nih.gov/pubmed/28656296
http://dx.doi.org/10.3892/mmr.2017.6848
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