Heart failure and myocardial infarction, as well as many other diseases, are characterized by significant metabolic dysfunction and cell death both of which have been shown to initiate and drive disease.  Mitochondrial calcium signaling is central to these processes regulating both oxidative phosphorylation (energy production) and cell death.  While much is known about how calcium exchange is regulated at the plasma membrane and ER/SR our understanding of the mitochondrial calcium microdomain remains elementary.  The lab utilizes in vitro and in vivo techniques ranging from real-time measurements of calcium exchange in isolated cells to surgical and genetic animal models of disease to decipher the role of this cellular microdomain in the progression of heart failure and myocardial infarction.