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Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model
Heart failure (HF) is the end stage of various cardiovascular diseases, with high morbidity and mortality, and is associated with a poor prognosis. One of the primary causes of HF is aortic valve disease, manifested by progressive aortic valve stenosis (AVS), resulting in increased left ventricular...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2022
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9581147/ https://www.ncbi.nlm.nih.gov/pubmed/36277751 http://dx.doi.org/10.3389/fcvm.2022.1028558 |
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author | Liu, Shaoyan Lan, Yang Zhao, Yun Zhang, Qianyu Lin, Tzuchun Lin, Kaibin Guo, Junjie Yan, Yan |
author_facet | Liu, Shaoyan Lan, Yang Zhao, Yun Zhang, Qianyu Lin, Tzuchun Lin, Kaibin Guo, Junjie Yan, Yan |
author_sort | Liu, Shaoyan |
collection | PubMed |
description | Heart failure (HF) is the end stage of various cardiovascular diseases, with high morbidity and mortality, and is associated with a poor prognosis. One of the primary causes of HF is aortic valve disease, manifested by progressive aortic valve stenosis (AVS), resulting in increased left ventricular load, ventricular hypertrophy, ultimately ventricular dysfunction, and HF. Early assessment of the degree of cardiomyopathy and timely intervention is expected to improve patients’ cardiac function and delay or even avoid the occurrence of HF. The Wnt signaling pathway is mainly involved in regulating myocardial insufficiency after valve stenosis. Connexin 43 protein (Cx43) is an essential target of Wnt signaling pathway that forms gap junction (GJ) structures and is widely distributed in various organs and tissues, especially in the heart. The distribution and transformation of Cx43 among cardiac cells are crucial for the development of HF. To specifically label Cx43 in vivo, we established a new Cx43-BFP-GFP mouse model with two loxp sites on both sides of the tag BFP-polyA box, which can be removed by Cre recombination. This double-reporter line endowed us with a powerful genetic tool for determining the area, spatial distribution, and functional status of Cx43. It also indicated changes in electrical conduction between cells in a steady or diseased state. |
format | Online Article Text |
id | pubmed-9581147 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-95811472022-10-20 Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model Liu, Shaoyan Lan, Yang Zhao, Yun Zhang, Qianyu Lin, Tzuchun Lin, Kaibin Guo, Junjie Yan, Yan Front Cardiovasc Med Cardiovascular Medicine Heart failure (HF) is the end stage of various cardiovascular diseases, with high morbidity and mortality, and is associated with a poor prognosis. One of the primary causes of HF is aortic valve disease, manifested by progressive aortic valve stenosis (AVS), resulting in increased left ventricular load, ventricular hypertrophy, ultimately ventricular dysfunction, and HF. Early assessment of the degree of cardiomyopathy and timely intervention is expected to improve patients’ cardiac function and delay or even avoid the occurrence of HF. The Wnt signaling pathway is mainly involved in regulating myocardial insufficiency after valve stenosis. Connexin 43 protein (Cx43) is an essential target of Wnt signaling pathway that forms gap junction (GJ) structures and is widely distributed in various organs and tissues, especially in the heart. The distribution and transformation of Cx43 among cardiac cells are crucial for the development of HF. To specifically label Cx43 in vivo, we established a new Cx43-BFP-GFP mouse model with two loxp sites on both sides of the tag BFP-polyA box, which can be removed by Cre recombination. This double-reporter line endowed us with a powerful genetic tool for determining the area, spatial distribution, and functional status of Cx43. It also indicated changes in electrical conduction between cells in a steady or diseased state. Frontiers Media S.A. 2022-10-05 /pmc/articles/PMC9581147/ /pubmed/36277751 http://dx.doi.org/10.3389/fcvm.2022.1028558 Text en Copyright © 2022 Liu, Lan, Zhao, Zhang, Lin, Lin, Guo and Yan. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cardiovascular Medicine Liu, Shaoyan Lan, Yang Zhao, Yun Zhang, Qianyu Lin, Tzuchun Lin, Kaibin Guo, Junjie Yan, Yan Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title | Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title_full | Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title_fullStr | Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title_full_unstemmed | Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title_short | Expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
title_sort | expression of connexin 43 protein in cardiomyocytes of heart failure mouse model |
topic | Cardiovascular Medicine |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9581147/ https://www.ncbi.nlm.nih.gov/pubmed/36277751 http://dx.doi.org/10.3389/fcvm.2022.1028558 |
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