Heart failure is the leading cause of mortality in the industrial world. Current therapies aim to minimize the extent of maladaptive remodeling. A wealth of basic and clinical studies implicate that overactivity of ß-adrenergic, angiotensin and aldosterone signaling contributes to pathologic remodeling and blockade of these pathways improves cardiac function and long term survival. Despite these interventions many patients will eventually progress to end stage heart failure and the need for cardiac transplantation is a common outcome. These unfortunate results underscore the need for an improved understanding of how the heart responds to injury, identification of novel drug targets and further development of such therapies. Our group has developed novel animal models of cardiac injury to study a critically important and poorly understood process, cardiac recovery. Using these models, we aim to uncover the molecular mechanisms governing this essential process and identify new therapeutics for the treatment of heart failure.

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Advanced heart failure, cardiac transplantation, circulatory assist devices.

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