Doxorubicin-induced cardiotoxicity and risk factors

Belger, Carl; Abrahams, Carmelita; Imamdin, Aqeela; Lecour, Sandrine

doi:10.1016/j.ijcha.2023.101332

Cited by 4 publications

(1 citation statement)

References 174 publications

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“…The publication, unfortunately, did not suggest a therapeutic procedure to achieve these goals. Belger and coworkers analyzed risk factors in relation to cardiotoxicity and concluded inconclusively that "a better understanding" would be desirable [15]. The same applies to surveillance programs based on epidemiological data [16,17].…”

Section: Standpoint Of Oncologists and Cardiologists In Relation To C...mentioning

confidence: 99%

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Moncayo,

Moncayo

2024

Preprint

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Cardiotoxicity is an unwanted side-effect arising from different medications. The term describes a diminution of heart function, affecting especially left ventricular ejection fraction, which can progress to heart failure. Pediatric oncology patients treated with drugs of the anthracycline group, e.g., doxorubicin, can evolve to heart failure patients in adult age. Nuclear Medicine imaging of fatty acid oxidation and glycolysis accurately describes normal and altered heart metabolism. The most common finding is a state of cardiac glycolysis, which is reflected by increased uptake of 18F-desoxyglucose (18F-FDG) at a time when fatty acid oxidation is decreased. Glycolysis has recently been recognized as being the result of coenzyme Q10 deficiency as part of adaptation to hypoxia. Low LEVF correlates with impaired fatty acid oxidation. This deficiency can arise from chemotherapy and radiation and can be corrected by supplementation. Drugs like enalapril can improve fatty acid utilization. We will review relevant Nuclear Medicine imaging studies as well as fundamental biochemical data that demonstrate this pathogenetic path.

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Section: Standpoint Of Oncologists and Cardiologists In Relation To C...mentioning

confidence: 99%

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Moncayo,

Moncayo

2024

Preprint

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Sex Differences in Doxorubicin‐Induced Cardiotoxicity: Insights from Transcriptome Analysis

Su,

Fu,

Xiao

et al. 2024

Advanced Therapeutics

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Male patients have a higher risk of cardiotoxicity following doxorubicin (DOX) treatment than female patients. However, how this difference occurs at the transcriptome level remains unclear, and the mechanisms underlying these differences are understudied. This study aimed to describe the transcriptional patterns of males and females after DOX treatment and explore the possible mechanisms of sexual differences in DOX‐induced cardiotoxicity. Following DOX treatment, male mice exhibit more severe heart damage than female mice. Transcriptome analysis of mice with and without DOX treatment showed that differentially expressed genes (DEGs) are significantly different between males and females. The majority of DEGs are sex‐specific, and more DEGs are identified in males than females. A number of genes, including the oxidation‐related genes Gdf15 and Rbm3, exhibited altered expression either in males or females. Some other genes, including the ferroptosis‐related gene Cd74, changed their expression levels in both sexes, but at different scales. Biochemical experiments suggested that cardiomyocyte oxidation and ferroptosis may contribute to the sexual dimorphism of DOX‐induced cardiotoxicity. In summary, this study shows that, after exposure to DOX, males and females respond differently regarding the expression of hundreds of genes, including Gdf15, Rbm3, and Cd74, possibly explaining the sexual differences in DOX‐induced cardiotoxicity.

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Dibenzazepine, a γ-Secretase Enzyme Inhibitor, Protects Against Doxorubicin-Induced Cardiotoxicity by Suppressing NF-κB, iNOS, and Hes1/Hey1 Expression

Badr,

Alotaibi,

El-Orabi

2024

Inflammation

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Doxorubicin-induced cardiotoxicity and risk factors

Cited by 4 publications

References 174 publications

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Identifying Hypoxia and Glycolysis in Chemotherapy- and Radiation-Induced Cardiotoxicity by Nuclear Medicine Diagnostic Imaging With 18F-Flurodeoxyglucose – Key Role of Coenzyme Q10 Deficiency in Acquired Mitochondrial Dysfunction

Sex Differences in Doxorubicin‐Induced Cardiotoxicity: Insights from Transcriptome Analysis

Dibenzazepine, a γ-Secretase Enzyme Inhibitor, Protects Against Doxorubicin-Induced Cardiotoxicity by Suppressing NF-κB, iNOS, and Hes1/Hey1 Expression

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