Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Xiaopeng Zhao1, Zheng Tian1, Mingli Sun2

  • 1College of Exercise and Health, Shenyang Sport University, Shenyang, Liaoning, 110102, China.

Cell Death Discovery
|July 26, 2023
PubMed

Insights

Doxorubicin is a vital anticancer drug, but its cardiotoxicity is a major issue. This study explores how targeting Nrf2 (Nuclear factor erythroid 2-related factor 2) can help prevent this doxorubicin-induced cardiotoxicity.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Cardiology

Background:

  • Doxorubicin is a crucial broad-spectrum anticancer agent.
  • Doxorubicin-induced cardiotoxicity presents a significant clinical challenge.
  • Oxidative stress, cell death, and inflammation are key pathological mechanisms involved.

Purpose of the Study:

  • To introduce the role of Nrf2 (Nuclear factor erythroid 2-related factor 2) in doxorubicin-induced cardiotoxicity.
  • To discuss the pathological mechanisms of doxorubicin-induced cardiotoxicity.
  • To summarize therapeutic strategies targeting Nrf2.

Main Methods:

  • Literature review on Nrf2's role in oxidative stress, cell death, and inflammation.
  • Analysis of studies investigating Nrf2 activation for preventing doxorubicin-induced cardiotoxicity.
  • Synthesis of information on therapeutic modalities targeting Nrf2.

Main Results:

  • Nrf2 plays a critical role in cellular defense against oxidative stress.
  • Nrf2 is implicated in the pathological pathways of doxorubicin-induced cardiotoxicity.
  • Activating Nrf2 has shown promise in ameliorating doxorubicin-induced cardiotoxicity.

Conclusions:

  • Nrf2 is a key mediator in the cellular response to doxorubicin.
  • Targeting Nrf2 represents a promising therapeutic avenue to mitigate doxorubicin-induced cardiotoxicity.
  • Further research into Nrf2-activating therapies is warranted for clinical application.

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