Abstract
Myocardial damage in cancer patients is emphasized as a cause of death; however, there are not many murine cachexia models to evaluate cancer-derived heart disorder. Using the mouse cachexia model that we established previously, we investigated myocardial damage in tumor-bearing mice. In cachexic mice, decreased heart weight and myocardial volume, and dilated left ventricular lumen, and atrophied cardiomyocytes were noted. The cardiomyocytes also showed accumulated 8-hydroxydeoxyguanosine, decreased leucine zipper and EF-hand-containing transmembrane protein-1, and increased microtubule-associated protein light chain3-II. Levels of tumor necrosis factor-α and high-mobility group box-1 proteins in the myocardium were increased, and nuclear factor κB, a signaling molecule associated with these proteins, was activated. When rat cardiomyoblasts (H9c2 cells) were treated with mouse cachexia model ascites and subjected to flux analysis, both oxidative phosphorylation and glycolysis were suppressed, and the cells were in a quiescent state. These results are in good agreement with those previously reported on cancerous myocardial damage. The established mouse cachexia model can therefore be considered useful for analyzing cancer-derived myocardial damage.
Highlights
Cachexia affects 40–80% of all patients with advanced cancer, especially those with pancreatic, gastric, and esophageal cancers [1,2,3]
Weight loss is an important phenotype of cachexia, weight loss in cancer patients is associated with myocardial atrophy [5, 6]
The weight of the fat pad and quadriceps was reduced to 20% and 45%, respectively, as compared to those of the control group (Figure 1C, 1D)
Summary
Cachexia affects 40–80% of all patients with advanced cancer, especially those with pancreatic, gastric, and esophageal cancers [1,2,3]. Weight loss is an important phenotype of cachexia, weight loss in cancer patients is associated with myocardial atrophy [5, 6]. Myocardial damage is a common cause of cancer death [7]. Cancer-derived myocardial impairment is a status wherein cardiac atrophy, remodeling, and dysfunction are integrated [8, 9]. Cancer-derived myocardial impairment is characterized by morphological alterations such as left ventricular (LV) wall thinning, decreased heart volume, myocardial fibrosis, and remodeling of the left ventricle as reported in gastrointestinal, pancreatic, and nonsmall cell lung cancer [8]. The causes of cancer-derived myocardial impairment might be the effects of cancer itself, background heart disease, and influence of cancer treatments; they have not been given much clinical importance, and specific treatment efforts are delayed [8]
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