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biochemistry and biophysics


Research Assistant Professor of Biochemistry and Biophysics
Assistant Director of Johnson Foundation
Director, EPR laboratory

1009B Stellar-Chance Labs
422 Curie Boulevard
Philadelphia, PA 19104-6059
215-898-5153 (Office); 215-898-5123 (Lab)

Ph.D. University of Tokyo (1998) Biochemistry and Neuroscience



Dr. Ogiso's ultimate research interest is mitochondrial energy metabolism in human health and disease. While the main role of mitochondria is to generate ATP, mitochondria perform many other critical functions including lipid/steroid synthesis, Ca2+ regulation, iron regulation, heme/iron-sulfur cluster synthesis, cell signaling cascades, and so on. Mitochondria are central to eukaryotic cell function and survival. Therefore, mitochondrial dysfunctions lead to a remarkably wide range of human diseases including heart failure, type 2 diabetes, and neuronal degenerative diseases. Dr. Ogiso’s current focus, complex I, is the entry enzyme of the mitochondrial respiratory chain. Complex I plays a central role in cellular aerobic energy metabolism. Presently, we are tackling one of the most challenging fundamental questions in bioenergetics: How is electron transfer is linked to vectorial H+ translocation in complex I? This question has remained unanswered even 30 years after Mitchell’s Nobel Prize for the chemiosmotic theory.

We are also interested in how to rescue complex I dysfunction. The most crucial and unique function of complex I is NADH oxidation. Impaired NADH oxidation in mitochondria leads to lactic acidosis, high NADH/NAD+ ratio, increased reactive oxygen species (ROS), and eventually, apoptosis. One effective strategy is a complementation of dysfunctional complex I with alternative NADH dehydrogenases which can fix altered NADH/NAD+ balance and protect cells from excessive ROS generation. We are now searching for another strategy to modulate NADH/NAD+ levels by investigating the NAD+ metabolism. NAD+ precursors have been shown to slow down aging and extend lifespan. Considering the pivotal role of NAD+ in the regulation of DNA repair, stress resistance, and cell death in addition to its role in cellular respiration and energy production, NAD+ synthesis through the kynurenine pathway and/or salvage pathway is an attractive target for therapeutic intervention in mitochondrial diseases.

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