The goal of the research in my laboratory is aimed at understanding the control of cardiac metabolism in health and disease. Cardiomyocytes are terminally differentiated cells and cell death leads to a functional loss of these cells. My laboratory is interested in the loss of cardiomyocytes by programmed cell death, or apoptosis, particularly with respect to the events initiated within the mitochondrion. Mitochondrial changes, including the release of cytochrome c and the loss of the mitochondrial specific lipid, cardiolipin, have been implicated as early events in apoptosis initiated by diverse stimuli. Of particular interest in my laboratory is the role that cardiolipin synthesis and metabolism has on the susceptibility of the cardiomyocyte to apoptosis. My laboratory is also interested in the role bacterial lipopolysaccharide (LPS) on cardiac function and metabolism. LPS, a component of bacterial cell walls, induces multiple organ responses and can lead to ultimately to toxic shock and death. One of the clinically important sequellae of LPS exposure is damage to the heart. The role of apoptosis in this cardiac damage is not clear and we seek to integrate our understanding of the induction of apoptosis with the immune response that LPS stimulates.
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