期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 93, 期 1, 页码 307-319出版社
IOS PRESS
DOI: 10.3233/JAD-221199
关键词
Alzheimer's disease; amyloid-beta; cardiomyocytes; coronary artery endothelial cells; metabolomics; mitochondria
The study investigated the effects of amyloid-beta (Aβ) 1-40 and Aβ1-42 on the metabolism of cardiomyocytes and coronary artery endothelial cells. The results showed that Aβ1-42 affected the metabolism of different amino acids, and disrupted fatty acid metabolism in both cell types. Lipid peroxidation was increased while mitochondrial respiration was decreased in response to Aβ1-42 in both cell types. This study revealed the disruptive effects of Aβ on lipid metabolism and mitochondrial function in cardiac cells.
Background: An increasing number of experimental and clinical studies show a link between Alzheimer's disease and heart diseases such as heart failure, ischemic heart disease, and atrial fibrillation. However, the mechanisms underlying the potential role of amyloid-beta (A beta) in the pathogenesis of cardiac dysfunction in Alzheimer's disease remain unknown. We have recently shown the effects of A beta 1- 40 and A beta 1- 42 on cell viability and mitochondrial function in cardiomyocytes and coronary artery endothelial cells. Objective: In this study, we investigated the effects of A beta 1- 40 and A beta 1- 42 on the metabolism of cardiomyocytes and coronary artery endothelial cells. Methods: Gas chromatography-mass spectrometrywas used to analyze metabolomic profiles of cardiomyocytes and coronary artery endothelial cells treated with A beta 1- 40 and A beta 1-42. In addition, we determined mitochondrial respiration and lipid peroxidation in these cells. Results: We found that the metabolism of different amino acids was affected by A beta 1- 42 in each cell type, whereas the fatty acid metabolism is consistently disrupted in both types of cells. Lipid peroxidation was significantly increased, whereas mitochondrial respiration was reduced in both cell types in response to A beta 1-42. Conclusion: This study revealed the disruptive effects of A beta on lipid metabolism and mitochondria function in cardiac cells.
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