Research Progress on the Mechanism, Monitoring, and Prevention of Cardiac Injury Caused by Antineoplastic Drugs—Anthracyclines

Figures

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  Figure 1. Schematic representation of anthracycline-induced oxidative stress. (A) Anthracyclines disrupt the mitochondrial electron transport chain, enhancing ROS generation. (B) Anthracyclines increase NADPH oxidase activity, accelerating electron transfer from NADPH to the plasma membrane and reducing O2 to form O2.−. (C) Anthracyclines uncouple eNOS, which in turn leads to decreased NO bioavailability and increased ROS production. (D) Anthracyclines cause intracellular iron overload in cardiomyocytes, and Fe2+ accumulation generates excessive ROS via the Fenton reaction.

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  Figure 2. Schematic diagram of anthracycline-induced apoptosis. (A) Anthracyclines activate the death receptor and form the death-inducing signaling complex. This complex subsequently activates the caspase cascade reaction, ultimately resulting in exogenous apoptosis. (B) BAX is activated to undergo a conformational change when anthracyclines stimulate the mitochondria, which leads to a decline in the mitochondrial membrane potential and the opening of the permeability transition pore. This event facilitates membrane lipid peroxidation and prompts the release of pro-apoptotic factors, notably Cyt c, which in turn triggers the caspase cascade reaction, leading to endogenous apoptosis.

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  Figure 3. Schematic diagram of anthracycline-induced changes in the cardiac microenvironment. Anthracyclines lead to the release of large amounts of inflammatory mediators, exacerbating the inflammatory response, contributing to the remodeling of the ECM, causing apoptosis or necrosis of cardiomyocytes, and further exacerbating the process of myocardial injury and fibrosis.

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  Figure 4. Schematic representation of anthracycline-induced ferroptosis. (A) Iron “overload” triggers the Fenton reaction, initiating ferroptosis. (B) Anthracycline-triggered alterations in the antioxidant system levels contribute to lipid peroxidation, which subsequently initiates the process of ferroptosis.

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  Figure 5. Schematic diagram of the prevention and treatment strategy for anthracycline-induced cardiotoxicity.