Molecular mechanism of doxorubicin-induced cardiomyopathy - An update

Eur J Pharmacol. 2018 Jan 5:818:241-253. doi: 10.1016/j.ejphar.2017.10.043. Epub 2017 Oct 23.

Abstract

Doxorubicin is utilized for anti-neoplastic treatment for several decades. The utility of this drug is limited due to its side effects. Generally, doxorubicin toxicity is originated from the myocardium and then other organs are also ruined. The mechanism of doxorubicin is intercalated with the DNA and inhibits topoisomerase 2. There are various signalling mechanisms involved in doxorubicin cardiotoxicity. First and foremost, the doxorubicin-induced cardiotoxicity is due to oxidative stress. Cardiac mitochondrial damage is supposed after few hours following the revelation of doxorubicin. This has led important new uses for the mechanism of doxorubicin-induced cardiotoxicity and novel avenues of investigation to determine better pharmacotherapies and interventions for the impediment of cardiotoxicity. The idea of this review is to bring up to date the recent findings of the mechanism of doxorubicin cardiomyopathies such as calcium dysregulation, endoplasmic reticulum stress, impairment of progenitor cells, activation of immune, ubiquitous system and some other parameters.

Keywords: Adriamycin; Cardiotoxicity; Doxorubicin; Oxidative stress; Signalling mechanism.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiomyopathies / chemically induced*
  • Cardiomyopathies / metabolism
  • Cardiomyopathies / pathology
  • Cell Death / drug effects
  • Doxorubicin / adverse effects*
  • Humans
  • Organelles / drug effects
  • Organelles / metabolism
  • Oxidative Stress / drug effects

Substances

  • Doxorubicin