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Heart Disease Link to Fetal Hypoxia and Oxidative Stress

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The quality of the intrauterine environment interacts with our genetic makeup to shape the risk of developing disease in later life. Fetal hypoxia is a common complication of pregnancy. It programmes cardiac and endothelial dysfunction in the offspring in adult life. However, the mechanisms via which this occurs remain elusive, precluding the identification of potential therapy. Using an integrative approach in large and small animal species at the in vivo, isolated organ, cellular and molecular levels, we proposed the hypothesis that oxidative stress in the fetal heart and vasculature underlies the mechanism via which prenatal hypoxia programmes cardiovascular dysfunction in later life. We show that developmental hypoxia independent of changes in maternal nutrition not only promotes fetal growth restriction or alters the trajectory of fetal growth, but it also induces changes in the cardiovascular, metabolic and endocrine systems of the adult offspring, which are normally associated with disease states during ageing (Camm et al. FASEB 25 (1):420, 2011; Giussani et al. PLoS One 7(2):e31017, 2012). Treatment with antioxidants, such as vitamin C, melatonin or allopurinol of animal pregnancies complicated with reduced oxygen delivery to the fetus prevents the alterations in fetal growth, and the cardiovascular, metabolic and endocrine dysfunction in the fetal and adult offspring. Our latest work shows the intergenerational inheritance of cardiovascular disease risk induced by chronic fetal hypoxia via the paternal line. Further, we show the intergenerational transmission of cardio-protection via the maternal mitochondria. Differential transmission of advantageous and detrimental traits onto offspring via either parental linage may provide a mechanism driving natural selection and successful environmental adaptation from generation to generation. Combined, the work offers both insight into mechanisms and possible therapeutic targets for clinical intervention against the early origin of disease in risky pregnancy across generations.

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