Research

Mitochondria control both cell survival and death. Healthy mitochondria produce the majority of cellular ATP and play a crucial role in metabolism, redox homeostasis, and signaling. Dysfunctional mitochondria generate toxic reactive oxygen species (ROS) and trigger programmed cell death. Multiple diseases (e.g., MELAS, Leigh syndrome, Parkinson’s disease) and aging are associated with defective mitochondria. In disease, a portion of the thousands of mitochondria in each cell is defective, which leads to cellular toxicity. Therefore, we hypothesize that selectively eliminating toxic, defective mitochondria will restore mitochondrial homeostasis and cellular physiology in disease. To test our hypothesis, we are developing chemical strategies to degrade defective mitochondria in primary mitochondrial disease and neurodegeneration.