A study of the epigenetic alterations that result in cardiac hypertrophy

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Heart disease is a significant cause of mortality in the developed world. In 2004 it was responsible for 137,700 deaths in the UK, equating to 24% of all deaths. A major predictor of mortality due to heart disease is cardiac hypertrophy (an increase in cell size without increase in cell number), and it is the most important risk factor for heart failure in humans. Hypertrophy can however also be a beneficial adaptive response providing the increased blood supply required during pregnancy and to sustain levels of increased physical activity experienced by athletes. Cardiac hypertrophy is characterised by an increase in the muscle mass/size of the heart due to enlargement of heart cells without any proliferation. This increase in heart size is caused by a significant change in the expression levels of a number of genes (the copying of DNA information into RNA and then oftern into protein). This remodelling of gene expression is controlled by factors (transcription factors) that bind to the DNA as well as by proteins that modify the structure and packaging of DNA. In this study, we plan to investigate the mechanisms that control suppression of gene transcription and whether these differ between the poorly reversible pathological forms of hypertrophy and the more reversible compensated hypertrophy.

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