Research Description:

There is growing evidence that many forms of cardiovascular disease (CVD) can be initiated by free radical mediated events which cause cellular damage. A cellular source and target of free radical production and damage is the mitochondrion. Because mitochondria are essential for multiple cell functions, including energy production, redox signaling, cell growth, proliferation, and programmed cell death, we hypothesize that free radicals cause mitochondrial damage and dysfunction in cells important in CVD development, and furthermore, that cardiovascular disease risk factors increase mitochondrial damage and dysfunction. Moreover, we hypothesize that fetal and/or childhood exposure to CVD risk factors increases the risk of adult disease development by causing mitochondrial damage and dysfunction. Finally, we also hypothesize that mitochondrial – nuclear interaction plays a significant role in individual disease susceptibility, and that environmentally influenced selection events for mitochondrial function that conveyed increased reproductive and survival success during the global establishment of human populations during prehistoric times, today, influences human disease susceptibility.

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