The role of toll-like receptors in myocardial toxicity induced by doxorubicin

Immunol Lett. 2020 Jan:217:56-64. doi: 10.1016/j.imlet.2019.11.001. Epub 2019 Nov 7.

Abstract

Doxorubicin is an effective antitumor drug commonly used in the treatment of a wide variety of cancers. However, doxorubicin may cause cardiac toxicity, which can cause congestive heart failure in severe cases, and this seriously limits its clinical application. It is believed that doxorubicin promotes the formation of reactive oxygen species, inducing oxidative stress, and at the same time, reduces the content of antioxidant substances in cardiac tissues, causing adverse effects. Toll-like receptors (TLRs) are biomolecules expressed on the surfaces of macrophages, dendritic cells, and epithelial cells that can recognize various types of pathogen-related or damage-related molecular patterns. In recent years, a large number of studies have confirmed that TLRs play important roles in the cardiac toxicity induced by doxorubicin. This review aimed to explore the role of TLRs in the cardiac toxicity induced by doxorubicin and provide possible solutions.

Keywords: Cardiotoxicity; Doxorubicin; Toll-like receptors.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibiotics, Antineoplastic / metabolism
  • Antibiotics, Antineoplastic / toxicity*
  • Apoptosis / drug effects
  • Cardiotoxicity / metabolism
  • DNA Damage / drug effects
  • Doxorubicin / metabolism
  • Doxorubicin / toxicity*
  • Heart / drug effects*
  • Humans
  • Mitochondria, Heart / drug effects
  • Mitochondria, Heart / metabolism
  • Mitochondria, Heart / pathology
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Reactive Oxygen Species / metabolism
  • Signal Transduction / drug effects*
  • Toll-Like Receptors / metabolism*

Substances

  • Antibiotics, Antineoplastic
  • Reactive Oxygen Species
  • Toll-Like Receptors
  • Doxorubicin