Editors' ChoiceCardiovascular Disease

An antioxidant to attenuate aortic aging

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Science Translational Medicine  15 Nov 2017:
Vol. 9, Issue 416, eaaq1235
DOI: 10.1126/scitranslmed.aaq1235

Abstract

Supplementation with the mitochondrial targeted antioxidant MitoQ for 4 weeks decreased aortic stiffness in old mice.

A common risk factor for many chronic, debilitating, and deadly diseases is advanced age. Currently, there are no therapies or technologies available to completely reverse aging related declines in metabolism, physiology, and health. However, interventions that address and attenuate oxidative and free radical stress, which has been historically seen as a major driving force in aging, pose potential treatment routes. Dietary antioxidants, such as vitamins C and E, while necessary for normal health and cellular homeostasis, have not proven to slow the aging process when supplemented at supposedly therapeutic levels. A possible reason for this is that general antioxidants are not able to reach and mitigate all reactive oxygen species (ROS) produced throughout our bodies and cells and, in particular, the ROS that drive the aging process. As mitochondria are linked to pathogenic ROS production, the development of mitochondria-targeted antioxidant therapies may have increased efficacy and potency for delaying and/or reversing the aging process.

One hallmark of the aging process is the stiffening and hardening of arteries. This places increased stress on the heart and other tissues and eventually leads to organ failure. In the recent study by Gioscia-Ryan et al., supplementation of a mitochondrial-targeted antioxidant in mice was tested as a means to reverse aging-related stiffening of the arteries, and more specifically, in the aorta. Four-week supplementation of MitoQ in the drinking water of 27-month-old mice was sufficient to decrease aortic stiffness, as measured by pulse-wave velocity, and improve aortic mechanical properties, as measured by elastic modulus of elastin region and elastin expression and stability. However, MitoQ supplementation did not diminish aging-related increases in proinflammatory cytokine expression. This suggests that the molecular mechanism of MitoQ–driven improvements in aortic elasticity was through sequestering of ROS and maintaining proper and effective levels of elastin and was independent of proinflammatory signaling. As arterial stiffening due to mitochondria-derived ROS is a driving factor of multiple aging-related diseases, future preclinical and clinical studies utilizing mitochondrial-targeted antioxidant therapies should be pursued to translate this antiaging intervention for human use.

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