The link between mitochondria damage, inflammation and atherosclerosis

Mitochondrial dysfunction, inflammation and treatment in atherosclerosis

In atherosclerosis, the blood vessels in our bodies ‘fur up’ with fatty plaque deposits and blood vessels narrow. If the blood flow supplying the heart or the brain becomes blocked or restricted, or if fatty plaques rupture, heart attacks and strokes can occur. Dr Emma Yu and colleagues at the University of Cambridge have discovered that defects in the DNA of mitochondria, the part of the cell that generates energy, promotes atherosclerosis in mice. They have also found that damage to mitochondrial DNA in white blood cells involved with inflammation is linked with higher-risk plaques that are more likely to rupture. The BHF has now awarded the team a grant to find out exactly how damage to mitochondria is linked to inflammation, how it promotes atherosclerosis and if improving mitochondrial function could reduce atherosclerosis. They will investigate whether mitochondria are defective in blood vessels in people with atherosclerosis, and if reducing this mitochondrial damage makes a difference to the disease by researching mice and human heart tissue samples. This study will reveal if improving the amount and quality of mitochondrial DNA could be a new way to treat atherosclerosis.