Abstract
A Similar Metabolic Profile Between the Failing Myocardium and Tumor Could Provide Alternative Therapeutic Targets in Chemotherapy-Induced Cardiotoxicity.
Highlights
BcrAbl kinase is a specific gene fusion that causes chronic myeologenous leukemia (CML) [4], and Bcr-Abl kinase inhibitors, including imatinib mesylate are effective in treating CML [5], they are associated with cardiotoxicity in pre-clinical animal studies and patients [6], suggesting that alternative adjuvant therapies that can prevent, limit or improve CIC need to be developed
The myocardium is the most energetically demanding organ of our body, and predominantly utilizes long-chain fatty acids and glucose as the primary substrates to generate adenosine triphosphate (ATP), which is required for myocardial contractility [14]
The normal myocardium generates the majority of its ATP (∼60–90%) from mitochondrial fatty acid β-oxidation (FAO) and glucose oxidation (GO), with cytoplasmic GLY providing a minimal alternative energy-producing pathway [14, 15]
Summary
BcrAbl kinase is a specific gene fusion that causes chronic myeologenous leukemia (CML) [4], and Bcr-Abl kinase inhibitors, including imatinib mesylate are effective in treating CML [5], they are associated with cardiotoxicity in pre-clinical animal studies and patients [6], suggesting that alternative adjuvant therapies that can prevent, limit or improve CIC need to be developed. Therapeutic Targets in Cardiotoxicity we will discuss metabolic pathways that appear to be induced in both the failing heart and tumor, suggesting that metabolic therapies could provide an alternative approach for treating CIC, without hindering or potentially even improving chemotherapyinduced tumor regression.
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