Studies have shown that following mitochondrial dysfunction, endothelial cells release large amounts of pro-inflammatory mediators such as IL-1, IL-6, and TNF-alpha and enhance the expression of intercellular adhesion molecule-1 (ICAM-1) that cause monocyte infiltration and activation (Choi S.J. et al., 2018). This evidence concerns the gene ICAM1 and Abnormality of mitochondrial metabolism.