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Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin
Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055600/ https://www.ncbi.nlm.nih.gov/pubmed/29665007 http://dx.doi.org/10.1002/jcp.26615 |
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author | Wang, Yu Cui, Xiaoxue Wang, Yilin Fu, Yao Guo, Xin Long, Jie Wei, Chengxi Zhao, Ming |
author_facet | Wang, Yu Cui, Xiaoxue Wang, Yilin Fu, Yao Guo, Xin Long, Jie Wei, Chengxi Zhao, Ming |
author_sort | Wang, Yu |
collection | PubMed |
description | Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a reduction in miR378* expression. Expression changes in calumenin, an endoplasmic reticulum stress (ERS) chaperone protein and pathway factor, as well as apoptosis, were observed in cardiomyocytes after doxorubicin‐induced injury. However, miR378* increased calumenin expression, eased ERS, and reduced cardiomyocyte apoptosis, while, silencing miR378* reduced calumenin expression, aggravated ERS, and increased cardiomyocyte apoptosis. The above results indicate that miR378* alleviates ERS and inhibits the activation of the ERS‐mediated apoptosis signaling pathway in cardiomyocytes via regulating calumenin expression, thereby reducing cardiomyocyte apoptosis after doxorubicin‐induced injury. Increasing miR378* expression may be a new way to improve cardiac function and quality of life in patients with Dox cardiomyopathy. |
format | Online Article Text |
id | pubmed-6055600 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-60556002018-07-23 Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin Wang, Yu Cui, Xiaoxue Wang, Yilin Fu, Yao Guo, Xin Long, Jie Wei, Chengxi Zhao, Ming J Cell Physiol Rapid Communications Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin‐induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a reduction in miR378* expression. Expression changes in calumenin, an endoplasmic reticulum stress (ERS) chaperone protein and pathway factor, as well as apoptosis, were observed in cardiomyocytes after doxorubicin‐induced injury. However, miR378* increased calumenin expression, eased ERS, and reduced cardiomyocyte apoptosis, while, silencing miR378* reduced calumenin expression, aggravated ERS, and increased cardiomyocyte apoptosis. The above results indicate that miR378* alleviates ERS and inhibits the activation of the ERS‐mediated apoptosis signaling pathway in cardiomyocytes via regulating calumenin expression, thereby reducing cardiomyocyte apoptosis after doxorubicin‐induced injury. Increasing miR378* expression may be a new way to improve cardiac function and quality of life in patients with Dox cardiomyopathy. John Wiley and Sons Inc. 2018-04-17 2018-10 /pmc/articles/PMC6055600/ /pubmed/29665007 http://dx.doi.org/10.1002/jcp.26615 Text en © 2018 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, 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 | Rapid Communications Wang, Yu Cui, Xiaoxue Wang, Yilin Fu, Yao Guo, Xin Long, Jie Wei, Chengxi Zhao, Ming Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title | Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title_full | Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title_fullStr | Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title_full_unstemmed | Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title_short | Protective effect of miR378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
title_sort | protective effect of mir378* on doxorubicin‐induced cardiomyocyte injury via calumenin |
topic | Rapid Communications |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6055600/ https://www.ncbi.nlm.nih.gov/pubmed/29665007 http://dx.doi.org/10.1002/jcp.26615 |
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