Endothelial dysfunction as a complication of anti-cancer therapy

Pharmacol Ther. 2022 Sep:237:108116. doi: 10.1016/j.pharmthera.2022.108116. Epub 2022 Jan 19.

Abstract

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 inflammation 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 approaches 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.

Keywords: Cancer-therapy related cardiac dysfunction; Cardio-oncology; Chemotherapy; Endothelium; Inflammation; Microcirculation.

Publication types

  • Review
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents* / adverse effects
  • Cardiotoxicity / etiology
  • Endothelium, Vascular
  • Humans
  • Microcirculation
  • Neoplasms* / drug therapy

Substances

  • Antineoplastic Agents