Visnagin:抗蒽环类药物毒性的新型心脏保护剂(综述)

Omar Obeidat, Ali Obeidat, Abedallah Obeidat, Mohamed Ismail
{"title":"Visnagin:抗蒽环类药物毒性的新型心脏保护剂(综述)","authors":"Omar Obeidat, Ali Obeidat, Abedallah Obeidat, Mohamed Ismail","doi":"10.3892/mi.2024.161","DOIUrl":null,"url":null,"abstract":". Doxorubicin (DOX), a cornerstone of cancer chemotherapy, is marred by its dose‑dependent cardiotoxicity, leading to cardiomyopathy and heart failure. The epidemi‑ ology of DOX‑related cardiotoxicity highlights its cumulative, progressive nature, with a significant impact on the health of patients. The pathophysiological mechanisms involve mitochondrial dysfunction, oxidative stress and disrupted calcium homeostasis in cardiomyocytes. Despite the search for effective cardioprotective strategies, current treatments offer limited efficacy. Visnagin emerges as a potential solution, known for its vasodilatory and anti‑inflammatory properties, and recent studies suggest its cardioprotective efficacy against DOX‑induced cardiotoxicity through mitochondrial protection, the modulation of key signaling pathways and the inhibition of apoptosis. The present review aimed to provide a comprehen‑ sive overview of the mechanisms of action of visnagin, as well as to provide experimental evidence, and potential integration into cancer treatment regimens, highlighting its promise as a novel therapeutic agent for managing cardiotoxicity in patients undergoing anthracycline chemotherapy.","PeriodicalId":74161,"journal":{"name":"Medicine international","volume":"120 32","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Visnagin: A novel cardioprotective agent against anthracycline toxicity (Review)\",\"authors\":\"Omar Obeidat, Ali Obeidat, Abedallah Obeidat, Mohamed Ismail\",\"doi\":\"10.3892/mi.2024.161\",\"DOIUrl\":null,\"url\":null,\"abstract\":\". Doxorubicin (DOX), a cornerstone of cancer chemotherapy, is marred by its dose‑dependent cardiotoxicity, leading to cardiomyopathy and heart failure. The epidemi‑ ology of DOX‑related cardiotoxicity highlights its cumulative, progressive nature, with a significant impact on the health of patients. The pathophysiological mechanisms involve mitochondrial dysfunction, oxidative stress and disrupted calcium homeostasis in cardiomyocytes. Despite the search for effective cardioprotective strategies, current treatments offer limited efficacy. Visnagin emerges as a potential solution, known for its vasodilatory and anti‑inflammatory properties, and recent studies suggest its cardioprotective efficacy against DOX‑induced cardiotoxicity through mitochondrial protection, the modulation of key signaling pathways and the inhibition of apoptosis. The present review aimed to provide a comprehen‑ sive overview of the mechanisms of action of visnagin, as well as to provide experimental evidence, and potential integration into cancer treatment regimens, highlighting its promise as a novel therapeutic agent for managing cardiotoxicity in patients undergoing anthracycline chemotherapy.\",\"PeriodicalId\":74161,\"journal\":{\"name\":\"Medicine international\",\"volume\":\"120 32\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-05-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Medicine international\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.3892/mi.2024.161\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medicine international","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3892/mi.2024.161","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

摘要

.多柔比星(DOX)是癌症化疗的基石,其剂量依赖性心脏毒性导致心肌病和心力衰竭。与 DOX 相关的心脏毒性的流行病学突显了其累积性和渐进性,对患者的健康产生了重大影响。其病理生理机制涉及线粒体功能障碍、氧化应激和心肌细胞钙平衡紊乱。尽管人们一直在寻找有效的心脏保护策略,但目前的治疗方法疗效有限。Visnagin 因其血管扩张和抗炎特性而闻名,最近的研究表明,它通过线粒体保护、调节关键信号通路和抑制细胞凋亡,对 DOX 引起的心脏毒性具有保护作用。本综述旨在全面概述粘菌素的作用机制,并提供实验证据,以及将粘菌素纳入癌症治疗方案的可能性,强调粘菌素有望成为控制蒽环类化疗患者心脏毒性的新型治疗药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Visnagin: A novel cardioprotective agent against anthracycline toxicity (Review)
. Doxorubicin (DOX), a cornerstone of cancer chemotherapy, is marred by its dose‑dependent cardiotoxicity, leading to cardiomyopathy and heart failure. The epidemi‑ ology of DOX‑related cardiotoxicity highlights its cumulative, progressive nature, with a significant impact on the health of patients. The pathophysiological mechanisms involve mitochondrial dysfunction, oxidative stress and disrupted calcium homeostasis in cardiomyocytes. Despite the search for effective cardioprotective strategies, current treatments offer limited efficacy. Visnagin emerges as a potential solution, known for its vasodilatory and anti‑inflammatory properties, and recent studies suggest its cardioprotective efficacy against DOX‑induced cardiotoxicity through mitochondrial protection, the modulation of key signaling pathways and the inhibition of apoptosis. The present review aimed to provide a comprehen‑ sive overview of the mechanisms of action of visnagin, as well as to provide experimental evidence, and potential integration into cancer treatment regimens, highlighting its promise as a novel therapeutic agent for managing cardiotoxicity in patients undergoing anthracycline chemotherapy.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信