Obeidat Omar, Obeidat Ali, Obeidat Abedallah, Ismail Mohamed F
Graduate Medical Education Program, College of Medicine, University of Central Florida, Orlando, FL 32816, USA.
Internal Medicine Residency Program, HCA Florida North Florida Hospital, Gainesville, FL 32605, USA.
Med Int (Lond). 2024 May 13;4(4):37. doi: 10.3892/mi.2024.161. eCollection 2024 Jul-Aug.
Doxorubicin (DOX), a cornerstone of cancer chemotherapy, is marred by its dose-dependent cardiotoxicity, leading to cardiomyopathy and heart failure. The epidemiology 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 comprehensive 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.
阿霉素(DOX)是癌症化疗的基石,但其剂量依赖性心脏毒性令人诟病,会导致心肌病和心力衰竭。阿霉素相关心脏毒性的流行病学凸显了其累积性、渐进性本质,对患者健康有重大影响。其病理生理机制涉及心肌细胞的线粒体功能障碍、氧化应激和钙稳态破坏。尽管一直在寻找有效的心脏保护策略,但目前的治疗效果有限。紫铆因作为一种潜在的解决方案崭露头角,它以其血管舒张和抗炎特性而闻名,最近的研究表明,它通过线粒体保护、关键信号通路的调节和细胞凋亡的抑制,对阿霉素诱导的心脏毒性具有心脏保护作用。本综述旨在全面概述紫铆因的作用机制,提供实验证据,并探讨其在癌症治疗方案中的潜在整合,突出其作为一种新型治疗药物在管理接受蒽环类化疗患者心脏毒性方面的前景。