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2000
Volume 32, Issue 15
  • ISSN: 0929-8673
  • E-ISSN: 1875-533X

Abstract

Introduction

Chemotherapy therapies are effective in treating cancer, but they can have harmful effects on the cardiovascular system. This study explores the possible role of metformin in reducing the cardiac damage caused by chemotherapy.

Methods

In this scoping review, we conducted a comprehensive literature search on electronic databases (PubMed, Scopus, and Web of Science (ISI)) until November 2023. The manuscript was screened regarding the role of metformin in chemotherapy-induced cardiotoxicity. Finally, 26 papers were selected after double screening.

Results

Chemotherapy has the potential to damage and cause cell death in the heart, resulting in molecular, biochemical, and histological changes compared to an untreated group. However, co-treatment with metformin may offer protection by preventing or reversing these harmful effects on cardiac cells. Metformin's cardioprotective properties are thought to be due to its ability to modulate oxidative stress, inflammation, autophagy, and the apoptotic pathway.

Conclusion

The present study strongly suggests that metformin is an effective solution to chemotherapy-induced cardiotoxicity. Metformin can alleviate the harmful effects of chemotherapy on the heart by affecting oxidative stress, inflammation, autophagy, and apoptosis pathways. However, it is essential to note that the use of metformin may have some drawbacks, as it is a non-targeted therapy and could potentially reduce the effectiveness of targeted cancer drugs. Despite this, the potential benefits of using metformin in clinical settings cannot be ignored. Further studies are necessary to determine the specifics of this interaction. Still, the promising results of this review suggest that metformin may be an essential tool in the fight against chemotherapy-induced cardiotoxicity.

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2024-08-16
2025-10-30
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  • Article Type:
    Review Article
Keyword(s): Cardiotoxicity; cisplatin; cyclophosphamide; doxorubicin; metformin; sunitinib
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