Antineoplastic Drug-Induced Cardiotoxicity: A Redox Perspective

Area of Science:

• Cardiology
• Oncology
• Biochemistry

Background:

• Antineoplastic drugs can induce cardiovascular toxicity (CTX), a significant side effect impacting cancer treatment.
• Multiple biochemical mechanisms underlie CTX, including alterations in cellular redox homeostasis due to reactive oxygen species (ROS) and reactive nitrogen species (RNS).

Purpose of the Study:

• To elucidate the mechanisms of antineoplastic drug-induced cardiovascular toxicity.
• To highlight the role of mitochondria and oxidative stress in CTX.
• To emphasize the need for effective cardioprotection strategies that do not compromise anticancer efficacy.

Main Methods:

• Review of biochemical studies identifying mechanisms of CTX.
• Analysis of cellular sources and subcellular components involved in redox homeostasis.
• Classification of CTX into Type 1 (irreversible injury) and Type 2 (reversible dysfunction).

Main Results:

• Chemotherapeutic agents disrupt redox homeostasis, increasing ROS/RNS production, with mitochondria being key targets.
• Type 1 CTX (e.g., anthracyclines) causes irreversible cardiac injury, while Type 2 CTX (e.g., targeted drugs) leads to reversible dysfunction.
• Oxidative/nitrosative reactions, alongside direct/indirect effects on cardiomyocytes and inflammatory cells, contribute to CTX.

Conclusions:

• Understanding CTX mechanisms is crucial for developing cardioprotective interventions.
• Integrated approaches using molecular, imaging, and clinical data can identify patients at risk.
• Further experimental and clinical studies are essential to balance the safety and efficacy of novel cancer therapies.