Aging adults are more likely to have—and die from—heart disease than their younger counterparts.
In a new study, researchers have found reasons to link biological aging to the development of narrowed, hardened arteries, independent of other risk factors like high cholesterol.
The research was conducted by a team at Michigan Medicine.
The team report aged mice had more severe atherogenesis than young mice, even when both groups had similar cholesterol levels for the same time period.
They identified a novel pathway within the aorta by which mitochondrial dysfunction and the pro-inflammatory cytokine IL-6 co-exist in a positive feedback loop with aging to increase atherosclerosis.
Future research may develop therapies to fight against the effects of vascular aging before high cholesterol becomes a problem, with the goal of reducing the development of atherogenesis in the first place.
One author of the study is Daniel Goldstein, M.D., of Michigan Medicine’s Frankel Cardiovascular Center.
The study is published in Circulation Research.
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