Beta-Amyloid Instigates Dysfunction of Mitochondria in Cardiac Cells

Alzheimer's disease (AD) includes the formation of extracellular deposits comprising aggregated beta-amyloid (A beta) fibers associated with oxidative stress, inflammation, mitochondrial abnormalities, and neuronal loss. There is an associative link between AD and cardiac diseases; however, the mechanisms underlying the potential role of AD, particularly A beta in cardiac cells, remain unknown. Here, we investigated the role of mitochondria in mediating the effects of A beta(1-40) and A beta(1-42) in cultured cardiomyocytes and primary coronary endothelial cells. Our results demonstrated that A beta(1-40) and A beta(1-42) are differently accumulated in cardiomyocytes and coronary endothelial cells. A beta(1-42) had more adverse effects than A beta(1-40) on cell viability and mitochondrial function in both types of cells. Mitochondrial and cellular ROS were significantly increased, whereas mitochondrial membrane potential and calcium retention capacity decreased in both types of cells in response to A beta(1-42). Mitochondrial dysfunction induced by A beta was associated with apoptosis of the cells. The effects of A beta(1-42) on mitochondria and cell death were more evident in coronary endothelial cells. In addition, A beta(1-40) and A beta(1-42) significantly increased Ca2+ -induced swelling in mitochondria isolated from the intact rat hearts. In conclusion, this study demonstrates the toxic effects of A beta on cell survival and mitochondria function in cardiac cells.

Automated summary

This study demonstrates the toxic effects of Aβ on cell survival and mitochondria function in cardiac cells, highlighting the different impacts of Aβ(1-40) and Aβ(1-42) and the association between mitochondrial dysfunction and cell apoptosis.