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The Kranias laboratory is focusing on the role of Ca2+-handling and Ca2+-signaling in the regulation of myocardial function and survival in health and disease. In particular, we are interested in unraveling the mechanisms underlying the impaired regulation of sarcoplasmic reticulum Ca2+-cycling in cardiac and skeletal myopathies to identify novel therapeutic targets. We are using an integrative approach with state-of-the-art techniques, spanning the molecular, biomedical, cellular, intact organ and intact animal levels. Our team has generated and characterized a large number of genetically altered mouse models, affording significant insights into the regulation of cardiac function, apoptosis, necrosis and autophagy. Importantly our laboratory studies have been extended from the bench to the clinic, including the identification of human variants in key Ca-cycling genes that may serve as potential prognostic or diagnostic markers for the development of arrhythmia and heart failure.
The overall goal of Dr. Kranias’ research program is to build a comprehensive understanding on the role of calcium cycling in cardiac contractility and cell survival.
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