Affiliations 

  • 1 Research Follower, INTI International University, 71800, Nilai, Negeri Sembilan, Malaysia. [email protected]
  • 2 Faculty of Business and Communications, INTI International University, 71800, Nilai, Negeri Sembilan, Malaysia
  • 3 Department of Pharmaceutical Microbiology, Faculty of Pharmacy, Delta State University, Abraka, Delta State, Nigeria
  • 4 Chandigarh Pharmacy College, Chandigarh Group of Colleges, Jhanjeri, Mohali, Punjab, 140307, India
  • 5 Department of Chemistry, NIMS Institute of Engineering & Technology, NIMS University Rajasthan, Jaipur, India
  • 6 Department of Basic Medical Sciences, College of Medicine, AlMaarefa University, Diriyah, 13713, Riyadh, Saudi Arabia. [email protected]
  • 7 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, 72388, Sakaka, Aljouf, Saudi Arabia
  • 8 Department of Psychotherapy, Pirogov Russian National Research Medical University, 117997, Moscow, Russia
  • 9 Department of Medical Laboratories Technology, AL-Nisour University College, Baghdad, Iraq
  • 10 Medical Laboratory Technique College, The Islamic University, Najaf, Iraq
Med Oncol, 2024 Sep 11;41(10):244.
PMID: 39259412 DOI: 10.1007/s12032-024-02494-3

Abstract

The likelihood of survival for cancer patients has greatly improved due to chemotherapy medicines. However, these antitumor agents might also have unfavorable effects on the cardiovascular system, which could result in sudden or gradual cardiac failure. The production of free radicals that result in oxidative stress appears to be the key mechanism by which chemotherapy-induced cardiotoxicity (CIC) happens. Reports suggest that the Sirtuin-1 (Sirt1)/Nuclear factor E2-associated factor 2 (Nrf2) signaling pathway has been considered an alternative path for counteracting cardiotoxicity by suppressing oxidative stress, inflammation, and apoptosis. This review concludes recent knowledge about CIC with a special focus on the anti-oxidative regulation properties of the Sirt1/Nrf2 pathway.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.