ISSN |
1949-8462 (online) |
Open Access |
This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/ |
Copyright |
©The Author(s) 2025. Published by Baishideng Publishing Group Inc. All rights reserved. |
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Publisher |
Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA |
Website |
http://www.wjgnet.com |
Category |
Medicine, Research & Experimental |
Manuscript Type |
Basic Study |
Article Title |
Mechanism of myocardial damage induced by doxorubicin via calumenin-regulated mitochondrial dynamics and the calcium–Cx43 pathway
|
Manuscript Source |
Unsolicited Manuscript |
All Author List |
He Shi, Song-Ao Yang, Ling-Yu Bai, Jian-Jun Du, Zhe Wu, Zhi-Hui He, Hao Liu, Jia-Yue Cui and Ming Zhao |
ORCID |
|
Funding Agency and Grant Number |
Funding Agency |
Grant Number |
Technology Development of Jilin Province |
No: 20190701069GH |
Natural Science Foundation of Inner Mongolia Autonomous Region |
No: 2018MS08036, No: 2017MS(LH)0824 |
|
Corresponding Author |
Ming Zhao, Chief Physician, MD, PhD, Professor, Department of Cardiovascular Medicine, Affiliated Hospital of Inner Mongolia Minzu University, No. 22 Holin He Street, Tongliao 028000, Inner Mongolia Autonomous Region, China. langzhe73@163.com |
Key Words |
Calumenin; Mitochondrial dynamics; Doxorubicin; Apoptosis; Ca2+ concentration; Cardiotoxicity |
Core Tip |
Doxorubicin (DOX) is an antitumor drug, with the main side effect being cardiotoxicity. This study investigated the time course and mechanism of DOX-induced myocardial injury by injecting DOX into rats and conducting cardiac electrophysiological tests and ultrastructural observations of myocardium. The results showed that DOX began to damage myocardial mitochondria as early as the second week after administration. The study clearly demonstrated that DOX causes calcium overload in myocardial cells by reducing calumenin expression, which in turn leads to myocardial cell apoptosis and arrhythmia. |
Publish Date |
2025-05-23 09:07 |
Citation |
<p>Shi H, Yang SA, Bai LY, Du JJ, Wu Z, He ZH, Liu H, Cui JY, Zhao M. Mechanism of myocardial damage induced by doxorubicin via calumenin-regulated mitochondrial dynamics and the calcium–Cx43 pathway. <i>World J Cardiol</i> 2025; 17(5): 104839</p> |
URL |
https://www.wjgnet.com/1949-8462/full/v17/i5/104839.htm |
DOI |
https://dx.doi.org/10.4330/wjc.v17.i5.104839 |