Mitochondrial DNA Damage, Oxidative Stress, And Atherosclerosis

The study found that mitochondrial DNA (mtDNA) damage preceded and worsened atherosclerosis in mice, not through increased reactive oxygen species (ROS) but by reducing mitochondrial respiratory activity and ATP levels, leading to cell apoptosis and plaque vulnerability. Human data from the VIVA trial confirmed that mtDNA lesions were linked to high-risk plaques. The research suggested that improving mitochondrial health might be a more effective treatment for atherosclerosis than using antioxidants.