Abstract
SummaryCardiotoxicity, defined as toxicity that affects the heart, is one of the most common adverse drug effects. Numerous drugs have been shown to have the potential to induce lethal arrhythmias by affecting cardiac electrophysiology, which is the focus of current preclinical testing. However, a substantial number of drugs can also affect cardiac function beyond electrophysiology. Within this broader sense of cardiotoxicity, this review discusses the key drug-protein interactions known to be involved in cardiotoxic drug response. We cover adverse effects of anticancer, central nervous system, genitourinary system, gastrointestinal, antihistaminic, anti-inflammatory, and anti-infective agents, illustrating that many share mechanisms of cardiotoxicity, including contractility, mitochondrial function, and cellular signaling.
Highlights
Concerns regarding cardiac safety are among the top reasons for drug withdrawal from clinical trials and the market
thromboxane A2 (TXA2) activation leading to cardiac remodeling, electrolyte imbalances hERG trafficking inhibition disruption of cardiomyocyte survival via Vascular endothelial growth factor (VEGF) signaling inhibition hERG trafficking inhibition TXA2 activation leading to cardiac remodeling, electrolyte imbalance unknown
We illustrate that many of these drug classes share modes of action on cardiac function and on adverse cardiac events, with cardiotoxicity frequently resulting from the simultaneous interruption of key myocardial functions and viabilities
Summary
Cardiotoxicity, defined as toxicity that affects the heart, is one of the most common adverse drug effects. Numerous drugs have been shown to have the potential to induce lethal arrhythmias by affecting cardiac electrophysiology, which is the focus of current preclinical testing. A substantial number of drugs can affect cardiac function beyond electrophysiology. Within this broader sense of cardiotoxicity, this review discusses the key drug-protein interactions known to be involved in cardiotoxic drug response. We cover adverse effects of anticancer, central nervous system, genitourinary system, gastrointestinal, antihistaminic, anti-inflammatory, and anti-infective agents, illustrating that many share mechanisms of cardiotoxicity, including contractility, mitochondrial function, and cellular signaling
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