Yang Lee, M.S.
Oxidative damage, which is the accumulation of reactive oxygen species (ROS) in cells, affects the aging process, and old age is a major risk factor for cardiovascular diseases. This phenomenon is well explained by “The Oxidative Stress Theory of Aging”, which explains that the life span of an organism is determined by the age-related loss of physiological function by the progressive cumulating of oxidative damage. This theory has been modified to “The Mitochondrial Theory of Aging”, which is the contribution of mitochondria to oxidative stress. Thus, oxidative damage to mitochondrial components leads to a decrease of cellular functions that eventually determine the life span of an organism.
Magnesium superoxide dismutase (MnSOD) is an essential mitochondrial antioxidant enzyme located in the mitochondrial matrix that rapidly modifies superoxide anions, which induce oxidative damage. Research studies showed that mitochondria have a central role in age-related cardiac diseases. Evidently, mitochondrial dysfunction due to age is strongly correlated with abnormal oxidative stress production from mitochondria. Previously, our laboratory found that increased fibrotic tissue and structure change (bigger heart size) in aged rats’ hearts induced cardiac stiffness and impaired cardiac contractility. Also, we showed that decreased MnSOD expression and activity in the hearts of senescent rats was directly associated with increased oxidative stress levels. Recently, we found that cardiac stiffness and structure change was prevented in old mice by reducing fibrotic tissue and preventing age dependent pathological enlargement of the heart (cardiac remodeling) when MnSOD was genetically overexpressed. These results indicate the significant role of MnSOD in the heart as a protector from age dependent oxidative stress.
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