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The Sirt1/Nrf2 pathway is a key factor for drug therapy in chemotherapy-induced cardiotoxicity: a Mini-Review

Suleiman Ibrahim Shelash Mohammad1,2, Asokan Vasudevan3, Felix Oghenemaro Enwa4

  • 1Research Follower, INTI International University, 71800, Nilai, Negeri Sembilan, Malaysia. dr_sliman73@aabu.edu.jo.

Medical Oncology (Northwood, London, England)
|September 11, 2024
PubMed

Insights

Chemotherapy can harm the heart, causing cardiotoxicity through oxidative stress. The Sirtuin-1/Nuclear factor E2-associated factor 2 pathway may protect against this damage by reducing oxidative stress.

Area of Science:

  • Cardiovascular Pharmacology
  • Oncology
  • Molecular Biology

Background:

  • Chemotherapy improves cancer survival but can cause cardiotoxicity, leading to heart failure.
  • Oxidative stress from free radical production is a primary mechanism of chemotherapy-induced cardiotoxicity (CIC).

Purpose of the Study:

  • To review current knowledge on chemotherapy-induced cardiotoxicity.
  • To highlight the role of the Sirtuin-1 (Sirt1)/Nuclear factor E2-associated factor 2 (Nrf2) pathway in mitigating CIC.

Main Methods:

  • Literature review of studies on chemotherapy-induced cardiotoxicity.
  • Analysis of research on the Sirt1/Nrf2 signaling pathway's role in oxidative stress and apoptosis.

Main Results:

  • Chemotherapy agents can induce significant cardiovascular damage.
  • The Sirt1/Nrf2 pathway demonstrates potential in suppressing oxidative stress, inflammation, and apoptosis associated with CIC.

Conclusions:

  • The Sirt1/Nrf2 pathway offers a promising therapeutic target for preventing or treating chemotherapy-induced cardiotoxicity.
  • Understanding the anti-oxidative properties of Sirt1/Nrf2 is crucial for managing cardiotoxicity in cancer patients.
Keywords:
CardiotoxicityChemotherapyOxidative stressSirt1/Nrf2 pathway

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