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Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway

Mediastinal cancer radiotherapy exposes the heart and causes myocardial injury. It is of utmost importance to identify effective prevention and treatment targets. In this study, the regulatory role of adropin (Ad) in radiation-induced myocardial injury (RIMI) was explored in mice. After C57BL/6 mice...

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Autores principales: Li, Bingda, Wang, Zhenhua, He, Yuanqiao, Chen, Tianpeng, Zhang, Yun, Yuan, Xingxing, Li, Ping
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9339421/
https://www.ncbi.nlm.nih.gov/pubmed/35923860
http://dx.doi.org/10.1155/2022/8230214
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author Li, Bingda
Wang, Zhenhua
He, Yuanqiao
Chen, Tianpeng
Zhang, Yun
Yuan, Xingxing
Li, Ping
author_facet Li, Bingda
Wang, Zhenhua
He, Yuanqiao
Chen, Tianpeng
Zhang, Yun
Yuan, Xingxing
Li, Ping
author_sort Li, Bingda
collection PubMed
description Mediastinal cancer radiotherapy exposes the heart and causes myocardial injury. It is of utmost importance to identify effective prevention and treatment targets. In this study, the regulatory role of adropin (Ad) in radiation-induced myocardial injury (RIMI) was explored in mice. After C57BL/6 mice were administered E0771 cells and received radiotherapy, the effects of exogenous Ad intervention on myocardial fibrosis, apoptosis, microvessel density, oxidative stress, and protein expression levels were observed. The results showed that exogenous Ad effectively improved cardiac function, suppressed oxidative stress, inhibited myocardial fibrosis, reduced myocardial apoptosis, and promoted microangiogenesis in RIMI mice. Ad also downregulated the expression levels of transforming growth factor β1 (TGF-β1), NADPH oxidase 4 (NOX4), and cleaved caspase 3 and upregulated the expression of phosphor-endothelial nitric oxide synthase (p-eNOS). However, the above-mentioned effects of Ad were significantly reversed in Ad(−/−) mice. Radiotherapy resulted in the downregulation of phosphor-vascular endothelial growth factor receptor (p-VEGFR2) and p-Akt in myocardial tissue, which were upregulated by Ad. However, after targeted inhibition of VEGFR2 with apatinib, the effect of Ad on improving RIMI was significantly reversed. Taken together, exogenous Ad significantly ameliorated RIMI by reducing oxidative stress, promoting microangiogenesis, and inhibiting myocardial fibrosis and apoptosis. The underlying molecular mechanism involved may be elucidated by activation of the VEGFR2/PI3K/Akt pathway.
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spelling pubmed-93394212022-08-02 Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway Li, Bingda Wang, Zhenhua He, Yuanqiao Chen, Tianpeng Zhang, Yun Yuan, Xingxing Li, Ping Oxid Med Cell Longev Research Article Mediastinal cancer radiotherapy exposes the heart and causes myocardial injury. It is of utmost importance to identify effective prevention and treatment targets. In this study, the regulatory role of adropin (Ad) in radiation-induced myocardial injury (RIMI) was explored in mice. After C57BL/6 mice were administered E0771 cells and received radiotherapy, the effects of exogenous Ad intervention on myocardial fibrosis, apoptosis, microvessel density, oxidative stress, and protein expression levels were observed. The results showed that exogenous Ad effectively improved cardiac function, suppressed oxidative stress, inhibited myocardial fibrosis, reduced myocardial apoptosis, and promoted microangiogenesis in RIMI mice. Ad also downregulated the expression levels of transforming growth factor β1 (TGF-β1), NADPH oxidase 4 (NOX4), and cleaved caspase 3 and upregulated the expression of phosphor-endothelial nitric oxide synthase (p-eNOS). However, the above-mentioned effects of Ad were significantly reversed in Ad(−/−) mice. Radiotherapy resulted in the downregulation of phosphor-vascular endothelial growth factor receptor (p-VEGFR2) and p-Akt in myocardial tissue, which were upregulated by Ad. However, after targeted inhibition of VEGFR2 with apatinib, the effect of Ad on improving RIMI was significantly reversed. Taken together, exogenous Ad significantly ameliorated RIMI by reducing oxidative stress, promoting microangiogenesis, and inhibiting myocardial fibrosis and apoptosis. The underlying molecular mechanism involved may be elucidated by activation of the VEGFR2/PI3K/Akt pathway. Hindawi 2022-06-29 /pmc/articles/PMC9339421/ /pubmed/35923860 http://dx.doi.org/10.1155/2022/8230214 Text en Copyright © 2022 Bingda Li et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Li, Bingda
Wang, Zhenhua
He, Yuanqiao
Chen, Tianpeng
Zhang, Yun
Yuan, Xingxing
Li, Ping
Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title_full Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title_fullStr Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title_full_unstemmed Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title_short Adropin Improves Radiation-Induced Myocardial Injury via VEGFR2/PI3K/Akt Pathway
title_sort adropin improves radiation-induced myocardial injury via vegfr2/pi3k/akt pathway
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9339421/
https://www.ncbi.nlm.nih.gov/pubmed/35923860
http://dx.doi.org/10.1155/2022/8230214
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