About Me
Decoding Mitochondrial Metabolism at the Molecular Level
My research aims to understand how extrinsic factors — such as excess nutrients and impaired blood flow — shape hepatic mitochondrial immunometabolism and to identify conserved molecular mechanisms that convert adaptive redox signals into drivers of disease.
I have dedicated my career to characterizing the topology, capacity, and substrate use of mitochondrial reactive oxygen species (mROS) production sites. There are at least 11 distinct sites within enzymes of the electron transport chain that can prematurely leak electrons to oxygen, generating superoxide and hydrogen peroxide. My work has been pivotal in mapping these under both physiological and pathological conditions.
In a pioneering approach, I co-characterized two novel classes of small molecules — S1QELs and S3QELs — that selectively suppress mROS production without impairing cellular bioenergetics. My most recent study identified a defect in hepatic CoQ synthesis as the driver of excess mROS in obese mice via reverse electron transport at complex I site IQ, establishing a strong translational foundation linking mitochondrial redox biology to fatty liver disease in humans.