Figure 2.

Relationship between mitochondria and atherosclerosis in the endothelium. Mitochondria play a key role in endothelium function, participating in several processes, such as nitric acid production, intracellular signaling, and cell death. Excessive reactive oxygen species (ROS) production leads to endothelium senescence, apoptosis, and atherosclerosis progression. Mitochondria can be damaged by oxLDL, ROS (mostly from mitochondrial origin), and the aging process. Damaged mitochondria release several mitochondrial components such as mtROS, cardiolipin and mtDNA which induce nod like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation, leading to inflammation by increasing interleukin 1β and 18 maturation. Chronic NLRP3 activation will eventually lead to more mitochondrial damage by promoting mitochondrial calcium influx. Also, higher ROS levels disrupt the NO balance by boosting mitochondrial arginase II activity and causing eNOS degradation. In endothelium, the reduction of NO levels may also promote endothelial dysfunction and atherosclerosis. Most of these ROS-derived alterations are prevented by antioxidants enzymes (green block arrows).