Visnagin: A novel cardioprotective agent against anthracycline toxicity (Review)

Abstract

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.

Keywords: anthracycline; cancer chemotherapy; cardioprotection; cardiotoxicity; doxorubicin; visnagin.

Figure 1

Chemical structure for visnagin and doxorubicin.

Figure 2

Schematic diagram illustrating the mechanisms of cardiotoxicity of DOX and cardioprotection of visnagin. DOX, doxorubicin; ETC, electron transport chain; ATP Syn, ATP synthase; ROS, reactive oxygen species; MDH, malate dehydrogenase; VIS, visnagin; SIRT1, sirtuin 1; TCA, tricarboxylic acid; CYP2A, cytochrome P450 2A.