Increased synthesis of mitochondrial DNA plays a crucial role in driving inflammation and atherosclerosis, suggests a new University of Pittsburgh study in Nature Communications.
By performing genetic and functional analyses of immune cells, called macrophages, in the vessel wall, researchers discovered a signaling mechanism governing the proinflammatory effect of mitochondrial DNA in exacerbating atherosclerosis, the buildup of plaque in artery walls, which can cause heart attack or stroke. The findings were consistent in both mice and humans.
“Atherosclerosis is a devastating disease that often results in a heart attack,” said senior author Partha Dutta, associate professor of medicine and of immunology at Pitt. “Despite aggressive cholesterol-lowering measures, some patients remain at a high risk of death because of residual inflammation. Our study identifies an essential molecular contributor of atherosclerotic development and proposes a new direction for the development of effective treatments.”
These treatments include targeting the genes responsible for this process, adds Niranjana Natarajan, co-first author and assistant professor of medicine at Pitt. “A targeted drug-delivery method using nanotechnology could be used to reduce inflammation in lipid plaques to prevent heart attack or stroke,” she said.