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Heart Failure

Chronic HF is one of the leading causes of morbidity and mortality in the United States.  Approximately 5 million people in the U.S. have HF and more than 287,000 die from HF-associated causes each year (7). While recent studies have revealed many novel mechanisms for cardiac hypertrophic growth and subsequent decompensation leading to failure, few new clinical therapies have been developed in the last decade.  Existing approaches are aimed primarily at blocking neurohormones, relieving symptoms, preventing hospitalization, and improving the quality of life of patients, yet have had little overall impact on mortality. Recent research has provided new and often unexpected insights into the molecular signaling pathways involved in the progression of the disease; however, HF remains a complex multi-factorial problem. One major limitation has been in the quantitative assessment of proteins and perhaps more importantly their post-translational modifications (PTMs) on a global level – a core strength at JHU – that would allow us to understand the interplay between the various subproteomes of cardiomyocytes. Therefore, this contract will focus on the quantitative analysis of PTMs in the cardiac myocyte. The development of new techniques and tools will allow us to overcome current limitations while we refine and apply of existing technology.