Mitochondria are multifaceted organelles central to numerous processes including energy metabolism, programmed cell death, and immunity. My research program aims to define how mitochondria function as central regulators of innate immune and inflammatory responses, and to characterize how mitochondria-immune crosstalk contributes to human disease and aging. I am particularly interested in delineating how mitochondrial genome (mtDNA) stress and sensing by the cGAS-STING pathway potentiate type I interferon and pro-inflammatory responses. My laboratory has made significant contributions to understanding how the mtDNA-cGAS-STING axis governs disease-promoting metabolic and immune rewiring in pre-clinical models of mitochondrial disease, heart failure, neurological disorders, and cancer.