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mitochondria; atherosclerosis; metabolic syndrome; obesity; hypertension The study of Mercer et al.1, published in this edition of Circulation Research, reports new evidence linking oxidative DNA damage, atherosclerosis and the metabolic syndrome. Although these relationships have been long proposed,2-4 many have criticized previous reports asking the rhetorical question of which came first “the chicken or the egg? ” Or more specific to the topic of Mercer et al.'s study, does oxidative DNA damage actively promote atherosclerosis (and/or metabolic syndrome) or is DNA damage a result of these abnormalities? Conceptually, the theory is attractive. DNA damage occurs often. Every time you walk outside from your office or laboratory to another building your skin is bombarded by UV irradiation. Were it not for the presence of robust and often redundant DNA repair systems, multiple layers of cells in your skin would be damaged. In some cases the cells apoptose. The causation between induced DNA damage and cellular apoptosis has been established for many different types of cells.5 In other cases, genomic DNA might be altered in such a way as to promote malignant transformation. Or, mitochondrial DNA could be damaged such
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Madamanchi et al. (2010) studied this question.
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