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Diabetes, Inflammation, and the Spread of Electricity in the Heart
(VTC)
Steven Poelzing, PhD
Research Associate Professor
Department of Bioengineering
University of Utah
Salt Lake City, Utah
Sudden cardiac death presumably due to ventricular arrhythmias is still a major cause of death. Ventricular arrhythmias can be precipitated by premature activity and conduction abnormalities. Dr. Poelzing's group proposes that the propensity and timing of premature activity is in large part dependent on intracellular sodium as well as intracellular calcium. Sympathetic stimulation can exacerbate sodium and calcium handling, particularly during disease. Interestingly, diabetes modulates the heart's response to sympathetic stimulation. Future research is aimed at understanding how diabetes affects sodium and calcium handling, and thereby premature activity during sympathetic stimulation. Once premature activity is initiated, it is thought to propagate from cell to cell via gap junctions. However, there is little agreement in the field on what degree of gap junctional uncoupling during disease is necessary to produce conduction abnormalities. Dr. Poelzing's group recently provided evidence that the amount of fluid between cells can modulate propagation dependence on gap junction. They seek to understand how inflammatory signals, particularly in diabetes, modulate gap junctions, the extracellular matrix, and cardiac conduction.
Hosted by: Michael J. Friedlander, PhD, Executive Director, Virginia Tech Carilion Research Institute
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