Research

Mitochondria are central regulators of both cell survival and death. Healthy mitochondria produce the majority of cellular ATP and play essential roles in metabolism, redox homeostasis, and signaling. In contrast, dysfunctional mitochondria generate toxic reactive oxygen species (ROS) and can trigger programmed cell death. Defective mitochondria are implicated in a range of diseases—including MELAS, Leigh syndrome, and Parkinson’s disease—as well as aging.

In disease states, a subset of the thousands of mitochondria within each cell becomes dysfunctional, contributing to cellular toxicity. We hypothesize that selectively eliminating defective mitochondria while promoting biogenesis to repopulate cells with healthy mitochondria will restore mitochondrial homeostasis and normal cellular physiology. To test this hypothesis, we are developing chemical strategies to accelerate the selective degradation and recycling of defective mitochondria in the context of primary mitochondrial disease, neurodegeneration, and aging.