Chemotherapy-induced cardiotoxicity is a significant concern in cancer treatment, as certain chemotherapeutic agents can have adverse effects on the cardiovascular system. This can lead to a range of cardiac complications, including heart failure, arrhythmias, myocardial dysfunction, pericardial complications, and vascular toxicity. Strategies to mitigate chemotherapy-induced cardiotoxicity may include the use of cardioprotective agents (e.g., dexrazoxane), dose adjustments, alternative treatment regimens, and the implementation of preventive measures, such as lifestyle modifications and the management of cardiovascular risk factors. Ginsenosides, the active compounds found in ginseng (Panax ginseng), have been studied for their potential cardioprotective effects in the context of chemotherapy-induced cardiotoxicity. In this review, we investigate the cardioprotective effect of ginsenosides in chemotherapy-induced cardiotoxicity. Ginsenosides have been shown to possess potent antioxidant properties, which can help mitigate the oxidative stress and inflammation associated with chemotherapy-induced cardiac injury. They can modulate the expression of antioxidant enzymes and reduce the production of reactive oxygen species, thereby protecting cardiomyocytes from damage. Ginsenosides can also inhibit apoptosis (programmed cell death) of cardiomyocytes, which is a key mechanism underlying chemotherapy-induced cardiotoxicity. Modulation of ion channels, improvement of lipid profiles, anti-platelet and anti-thrombotic effects, and promotion of angiogenesis and neovascularization are another important mechanisms behind potential effects of ginsenosides on cardiovascular health. Ginsenosides can improve various parameters of cardiac function, such as ejection fraction, fractional shortening, and cardiac output, in animal models of chemotherapy-induced cardiotoxicity. The cardioprotective effects of ginsenosides have been observed in preclinical studies using various chemotherapeutic agents, including doxorubicin, cisplatin, and 5-fluorouracil. However, more clinical studies are needed to fully elucidate the therapeutic potential of ginsenosides in preventing and managing chemotherapy-induced cardiotoxicity in cancer patients.
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http://dx.doi.org/10.1186/s12938-024-01322-z | DOI Listing |
Biomed Eng Online
December 2024
Department of Stem Cells Technology and Tissue Regeneration, Faculty of Interdisciplinary Science and Technologies, Tarbiat Modares University, Tehran, 15614, Iran.
Chemotherapy-induced cardiotoxicity is a significant concern in cancer treatment, as certain chemotherapeutic agents can have adverse effects on the cardiovascular system. This can lead to a range of cardiac complications, including heart failure, arrhythmias, myocardial dysfunction, pericardial complications, and vascular toxicity. Strategies to mitigate chemotherapy-induced cardiotoxicity may include the use of cardioprotective agents (e.
View Article and Find Full Text PDFAnn Med Surg (Lond)
December 2024
Almanhal Academy for Science, Khartoum, Sudan.
Background: Chemotherapy-induced cardiotoxicity (CIC) is a significant challenge in cancer treatment, leading to heart failure and myocardial infarction. With rising cancer survival rates, the long-term cardiovascular health of survivors has gained importance. While several cardioprotective medications have been studied to mitigate chemotherapy's harmful effects on the heart, more research is needed to confirm their effectiveness and optimal use.
View Article and Find Full Text PDFCardiooncology
December 2024
Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Chemotherapy is one of the routine treatment for preventing rapid growth of the tumor cells. However, chemotherapeutic agents, especially doxorubicin cause damages to the normal cells especially cardiomyocytes. Cardiotoxicity induced by chemotherapeutic drugs lead to the myocardial cell injury and finally causes left ventricular dysfunction.
View Article and Find Full Text PDFClin Sci (Lond)
November 2024
Toronto General Hospital Research Institute, University Health Network, 100 College St., Toronto, Ontario Canada, M5G 1L7.
To maintain homeostasis in the heart, endothelial cells and cardiomyocytes engage in dynamic cross-talk through paracrine signals that regulate both cardiac development and function. Here, we review the paracrine signals that endothelial cells release to regulate cardiomyocyte growth, hypertrophy and contractility, and the factors that cardiomyocytes release to influence angiogenesis and vascular tone. Dysregulated communication between these cell types can drive pathophysiology of disease, as seen in ischemia-reperfusion injury, diabetes, maladaptive hypertrophy, and chemotherapy-induced cardiotoxicity.
View Article and Find Full Text PDFMol Cell Biochem
November 2024
Fangshan Hospital Beijing University of Chinese Medicine, Beijing, 102400, China.
Chemotherapy-induced cardiotoxicity is a major adverse effect, driven by multiple factors in its pathogenesis. Notably, RNAs have emerged as significant contributors in both cancer and heart failure (HF). RNAs carry genetic and metabolic information that mirrors the current state of cells, making them valuable as potential biomarkers and therapeutic tools for diagnosing, predicting, and treating a range of diseases, including cardiotoxicity.
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