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Cardioprotection in Drug-Induced Cardiotoxicity

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Guest Editor
Department of Pharmacology & Therapeutics, School of Medicine, College of Medicine and Health, University College Cork, T12 K8AF Cork, Ireland
Interests: cardioprotection; Cardiooncology; heart failure; myocardial infarction; ischemia-reperfusuin; phospholipid metabolism

Special Issue Information

Dear Colleagues,

More people are surviving cancer due to improved screening programmes and treatment options; however, many of these survivors go on to develop cardiac problems because of the drugs used to treat their cancer. This increased survival has highlighted the negative impact of some anticancer drugs on the heart. For example, Doxorubicin (Adriamycin), Fluoropyrimidines, and immune checkpoint inhibitors are effective drugs in the treatment of cancer, but they have been linked to significant cardiotoxic effects which affect morbidity and mortality. For many of these cancers, there is no equally effective alternative drug. Thus, an option is to cotreat these patients with an agent that minimises cardiotoxicity. However, very few such agents exist.

This Special Issue seeks to explore novel cardioprotective targets for drug-induced cardiotoxicity as well as innovative strategies for identifying and investigating cardioprotective agents in drug-induced cardiotoxicity. A better understanding of molecular mechanisms together with innovative solutions will help to shape the future of pharmacotherapy. This Special Issue welcomes review articles and primary research on the following (or related) topics:

  1. Novel molecular drug targets for protecting the heart in drug-induced cardiotoxicity (including, but not limited to, RNA therapeutics, epigenetic targets, gut–microbiome interactions, etc.);
  2. New approaches to existing molecular targets used to protect the heart in drug-induced cardiotoxicity;
  3. Novel methods and models for the identification of molecules and pathways that can protect the heart in drug-induced cardiotoxicity (including, but not limited to, computational methods, cell models, novel molecular methods, pharmacogenomics, etc.).

Dr. Roisin Kelly-Laubscher
Guest Editor

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Keywords

  • cardioprotection
  • cardiotoxicity
  • anthracycline
  • cardiac dysfunction
  • heart failure

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Published Papers (1 paper)

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Research

18 pages, 519 KiB  
Article
Drugs Metabolism-Related Genes Variants Impact on Anthracycline-Based Chemotherapy Induced Subclinical Cardiotoxicity in Breast Cancer Patients
by Domas Vaitiekus, Gintare Muckiene, Dovydas Verikas, Audrone Vaitiekiene, Skaiste Astasauskaite, Rolandas Gerbutavicius, Agne Bartnykaite, Rasa Ugenskienė, Renaldas Jurkevičius and Elona Juozaitytė
Int. J. Mol. Sci. 2025, 26(9), 4051; https://doi.org/10.3390/ijms26094051 - 25 Apr 2025
Viewed by 101
Abstract
Breast cancer is the most common cancer in women worldwide. Anthracyclines (doxorubicin, epirubicin, daunorubicin, idarubicin) are among the most used drugs for the treatment of breast cancer. Unfortunately, anthracyclines cause cardiotoxicity, which is a limiting factor for its use, and the lifetime cumulative [...] Read more.
Breast cancer is the most common cancer in women worldwide. Anthracyclines (doxorubicin, epirubicin, daunorubicin, idarubicin) are among the most used drugs for the treatment of breast cancer. Unfortunately, anthracyclines cause cardiotoxicity, which is a limiting factor for its use, and the lifetime cumulative dose of anthracyclines is the major risk factor for cardiotoxicity. In our study, we focused on acute and subacute heart damage. One of the main factors is a genetic predisposition, which determines individual susceptibility to anthracycline cardiotoxicity. The main idea of this study was, for the first time, to evaluate drug metabolism-related genes as a risk factor for developing cardiovascular toxicity in breast cancer patients. The main objective of our study was to identify the impact of drug metabolism-related gene SNPs on the development of subclinical heart damage during and/or after doxorubicin-based chemotherapy in breast cancer patients. The data of 81 women with breast cancer treated with doxorubicin-based chemotherapy in an outpatient clinic were analyzed, and SNP RT-PCR tests were performed. The drug metabolism-related gene variants SULT2B1 rs10426377, UGT1A6 rs17863783, CBR1 rs9024, CBR3 rs1056892, NCF4 rs1883112, and CYBA rs1049255 did not reach a statistically important impact on ABCC in multivariate logistic regression analysis. However, we identified that NCF4 rs1883112 had a risk reduction tendency for ABCC (OR = 0.49, 95% CI 0.27–0.87, p = 0.015). Our findings suggest that some SNPs, such as NCF4 rs1883112, may be associated with a reduced risk of cardiotoxicity, while no variants in this study showed a statistically significant increased risk. Even though, NCF4 rs1883112 showed a risk reduction tendency, suggesting the potential for personalized risk stratification. We can conclude that multiple genes are involved in ABCC, with different impacts, and it is unlikely that there is a single driver gene in ABCC pathogenesis. Full article
(This article belongs to the Special Issue Cardioprotection in Drug-Induced Cardiotoxicity)
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