My lab studies the role of mitochondria in generating, signaling, and responding to cellular stress, particularly in cardiac and skeletal muscle. In particular, we currently focus on how the dysregulation of mitochondrial calcium leads to physiological changes in mouse models. Mitochondrial calcium handling plays a critical role in energy production as well as cell death. To decipher the impact of calcium perturbation on multiple scales, our approaches span a variety of experimental techniques, from biochemical measurements on isolated mitochondria to live cell microscopy to in vivo phenotyping.