Spontaneous experimental atherosclerosis in hypercholesterolemic mice advances with ageing and correlates with mitochondrial reactive oxygen species

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Ageing and atherosclerosis are associated with oxidative stress. Mitochondrial redox function declines with ageing. Here we tested whether ageing LDL receptor knockout mice (LDLr−/−) develop spontaneous atherosclerosis and whether mitochondrial reactive oxygen species (mtROS) correlate with atherosclerosis. Compared with young mice, aged LDLr−/− mice exhibited 20-fold larger aortic lesion size, although the plasma cholesterol levels did not vary between age groups. The lesion sizes increased exponentially from 3 to 24 months of age (r = 0.92, p = 0.0001) and were correlated with mtROS across the age range (r = 0.81, p = 0.0001). Thus, LDLr−/− mice develop spontaneous diet-independent atherosclerosis, that advances exponentially with ageing. We propose that age related increases in mtROS contribute to accelerate atherosclerosis development in hypercholesterolemic mice.HighlightsLDLr−/− mice develop spontaneous diet-independent atherosclerosis.Atherosclerosis advances exponentially with ageing.Mitochondrial ROS levels correlate with ageing.Atherosclerosis development correlates with mitochondrial ROS levels during ageing.

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