- 1989-1993 B.A. - Biology, Kalamazoo College, Kalamazoo, MI
- 1993-2000 Ph.D. - Physiology, Stanford University, Stanford, CA
- 2000-2005 Postdoctoral Fellow, University of Washington, Seattle, WA
Mitochondria play a key role in integrating cellular energetics and the control of cell survival. As a result they are a critical element in aging and many degenerative diseases. We believe that an integrated study of mitochondrial energetics in the living organism is required for a mechanistic understanding of the role mitochondria play in degenerative disease. To that end, we have developed novel methods to directly measure mitochondrial function in vivo. Optical and magnetic resonance spectroscopies provide independent measures of oxygen and ATP fluxes in the intact animal. By independently measuring these fluxes we determine several parameters of mitochondrial energetics in skeletal muscle, including the coupling of ATP production to oxygen consumption. We have found that mitochondria in mouse skeletal muscle become less efficient with age, which results in a reduction in the ATP produced per oxygen consumed. This reduced efficiency can lead to an energetic stress on the cell and may impact cell survival. We combine these novel in vivo tools with detailed biochemical analyses of isolated mitochondria and permeabilized muscle fibers. By combining these approaches we are able to integrate the physiological relevance of our in vivo approach with the mechanistic detail available from ex vivo assays.
The focus of our current research is:
1) identifying the role of in vivo mitochondrial dysfunction and loss of energy homeostasis in pathophysiology of aging and disease,
2) the role of mitochondrial toxicity in the pathology associated with multiple xenobiotic compounds such as chemotherapeutic agents, environmental toxins and other drugs.