Endothelial dysfunction as a complication of anti-cancer therapy

Recent strides in anti-cancer therapeutics have improved longevity and led to a growing population of cancer survivors, who are increasingly likely to die of other causes. Treatment-induced cardiotoxicity is a complication of several therapeutic agents with acute and long-term consequences for cancer patients. Vascular endothelial dysfunction is a precursor and hallmark of ischemic coronary disease and may play a role in anti-cancer therapy-induced cardiotoxicity. This review summarizes clinical evidence for endothelial dysfunction following anti-cancer therapy and extends the discussion to include the impact of therapeutic agents on conduit arteries and the microcirculation. We highlight the role of innate immune system activation and cross-talk between in-flammation and oxidative stress as pathogenic mechanisms underlying anti-cancer therapy-induced vascular toxicity. Understanding the impact of anti-cancer agents on the vascular endothelium will inform therapeutic ap-proaches to prevent or reverse treatment-induced cardiotoxicity and may serve as an important tool to predict, monitor, and prevent adverse cardiovascular outcomes in patients undergoing treatment.(c) 2022 Elsevier Inc. All rights reserved.

Automated summary

Recent advances in anti-cancer therapeutics have improved the survival of cancer patients and led to an increasing number of cancer survivors dying from other causes. However, treatment-induced cardiotoxicity is a complication with acute and long-term consequences for cancer patients. This review summarizes the clinical evidence for endothelial dysfunction following anti-cancer therapy and discusses the impact of therapeutic agents on the blood vessels, highlighting the underlying pathogenic mechanisms of treatment-induced vascular toxicity.