Updates on Anticancer Therapy-Mediated Vascular Toxicity and New Horizons in Therapeutic Strategies

Area of Science:

• Oncology
• Cardiology
• Vascular Biology

Background:

• Vascular toxicity is a common side effect of anticancer chemotherapies, often stemming from endothelial cell (EC) dysfunction.
• Various treatments, including vascular endothelial growth factor inhibitors (VEGFi), anthracyclines, plant alkaloids, alkylating agents, antimetabolites, and radiation, can induce vascular toxicity.
• Cardiac ECs are crucial for cardiovascular functions, and their damage contributes to myocardial infarction, atherothrombosis, microangiopathies, and hypertension.

Purpose of the Study:

• To provide a comprehensive review of how chemotherapeutic agents induce vascular toxicity.
• To explore the impact of this toxicity on hypertension, microvascular rarefaction, thrombosis, atherosclerosis, and drug delivery.
• To describe potential therapeutic strategies for maintaining endothelial function during cancer treatment.

Main Methods:

• Literature review of studies on chemotherapy-induced vascular toxicity.
• Analysis of the mechanisms by which chemotherapeutic agents damage endothelial cells.
• Examination of therapeutic approaches to mitigate vascular toxicity.

Main Results:

• Chemotherapeutic agents damage cardiac ECs through various mechanisms, including inhibiting proliferation and altering vascular tone.
• This EC damage contributes to significant cardiovascular complications and affects the efficacy of drug delivery.
• Potential therapeutic strategies involve agents like vascular endothelial growth factor (VEGF)-B and prokineticin receptor-1 agonists.

Conclusions:

• Chemotherapy-induced vascular toxicity is a significant clinical challenge, impacting both patient health and treatment outcomes.
• Maintaining endothelial function is critical for managing cardiovascular risks associated with cancer therapy.
• Targeted therapies offer promise in preserving endothelial integrity without hindering anti-cancer efficacy.