Increased Mitochondrial DNA Copy Number Slows Vascular Aging in Mice

We examined multiple parameters of vascular function, histological markers, and markers of mitochondrial damage and function during normal vascular aging, and the effects of reducing or augmenting mitochondrial function on the onset and progression of vascular aging. We identify early, standardized time points and reproducible physiological parameters for vascular aging studies in mice. Vascular aging begins at far earlier time points than previously described in mice, with compliance, distensibility, stiffness, and pulse wave velocity (PWV) being the best discriminators for normal aging and manipulations. Mitochondrial DNA copy number and mitochondrial respiratory function are reduced when functional and structural manifestations of vascular aging begin. Rescue of the copy number deficit observed in normal aging improves mitochondrial respiration and delays all parameters of vascular aging, while reduced mtDNA integrity accelerates vascular aging. Together these data highlight the direct role of mtDNA-mediated mitochondrial dysfunction in the progression of vascular aging. Link: https://doi.org/10.1111/acel.12773
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