Abstract
Lipotoxicity is known to cause cellular dysfunction and death in non-adipose tissue. A major cause of lipotoxicity is the accumulation of saturated free fatty acids (FFA). Palmitic acid (PA) is the most common saturated fatty acid found in the human body. Endothelial cells form the blood vessels and are the first non-adipose cells to encounter FFA in the bloodstream. FFA overload has a direct impact on metabolism, which is evident through the changes occurring in mitochondria. To study these changes, the PA-treated human coronary artery endothelial cell (HCAEC) dataset was obtained from the Gene Expression Omnibus (GEO), and it was analyzed to obtain differentially expressed genes (DEGs) from the nucleus and mitochondria. Functional and pathway enrichment analyses were performed on DEGs. Results showed that nuclear and mitochondrial DEGs were implicated in several processes, e.g., reactive oxygen species (ROS) production, mitochondrial fusion and fission, Ca(2+) sequestering, membrane transport, the electron transport chain and the process of apoptosis. To better understand the role of FFA in endothelial cell damage, these DEGs can lead to future experiments based on these findings.