Document Type : Review Article
Authors
1
Thalassemia & Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
2
IIAIGC Study Center, Burlington, United States.
3
Student Research Committee, Ahvaz Jundishapur University of Medical Science, Ahvaz, Iran.
4
Thalassemia & Hemoglobinopathy Research Center, Health Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. & Student Research Committee, Ahvaz Jundishapur University of Medical Science, Ahvaz, Iran.
10.32598/ARI.81.1.3165
Abstract
Doxorubicin is a chemotherapeutic agent widely recognized for its efficacy in cancer treatment but also associated with a significant risk of inducing cardiomyopathy, both acutely and over the long term. The underlying mechanisms of myocardial damage involve the generation of reactive oxygen species (ROS), myocardial infiltration by neutrophils, elevated levels of myeloperoxidase (MPO) and tumor necrosis factor-alpha (TNF-α), as well as an increase in cardiac xanthine oxidase (XO) activity. This review presents and evaluates the burgeoning field of interventions aimed at reducing the cardiotoxicity associated with doxorubicin, a potent chemotherapeutic agent. To mitigate doxorubicin-induced cardiotoxicity, we introduce a novel therapeutic approach termed the dapsone, febuxostat, telmisartan (DFT) therapy. This regimen involves the administration of dapsone, febuxostat, and telmisartan—compounds known for their cardioprotective effects. This review synthesizes findings from the literature, detailing how each component of the DFT regimen contributes to cardioprotection through mechanisms such as the attenuating oxidative stress and inflammation, and modulating cardiac enzyme activities. Research on the DFT regimen has yielded encouraging outcomes in attenuating doxorubicin-induced cardiotoxicity. Dapsone, febuxostat, and telmisartan, both individually and in combination, have demonstrated a capacity to protect the heart by inhibiting ROS production, diminishing neutrophil infiltration, reducing levels of MPO and TNF-α, and suppressing XO activity. Furthermore, these agents are implicated in preserving cardiac function, preventing myocardial injury, and averting adverse remodeling. The DFT therapy presents a promising approach to reducing the cardiotoxic effects associated with doxorubicin in cancer patients. The collective evidence suggests that the DFT regimen not only attenuates doxorubicin-induced cardiotoxic effects but also preserves cardiac function, prevents myocardial injury, and averts adverse remodeling, underscoring its potential as an adjunctive therapy. Nonetheless, further preclinical and clinical studies are essential to confirm the cardioprotective efficacy of this regimen and to refine its application in oncology.
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