Toren Finkel received his undergraduate degree in physics from the University of Maryland before obtaining his M.D. and Ph.D. from Harvard Medical School in 1986. He completed his internship and residency training in internal medicine at the Massachusetts General Hospital in Boston, followed by a fellowship in cardiology at Johns Hopkins Medical School. In 1992, upon completion of this clinical training, he joined the NHLBI as an Investigator in the Cardiology Branch. He currently directs the Center for Molecular Medicine at NHLBI. Dr. Finkel is the author or coauthor of more than 200 publications. He is a former Senior Scholar of the Ellison Medical Foundation and serves as an editor or an editorial board member of Aging Cell, Mechanisms of Ageing and Development, Antioxidants and Redox Signaling, Molecular Aspects of Medicine, IUBMB Life and Science Magazine. He was inducted into the American Society of Clinical Research in 2002, the Association of American Physicians in 2009, and as a Fellow of the American Association for the Advancement of Science (AAAS) in 2013.
Dr. Finkel’s research is focused on the role of cellular metabolism and oxidative stress in aging and age-related diseases. He became interested in oxidative stress through an early, counterintuitive discovery that hydrogen peroxide—a reactive oxygen species (ROS)—could act as an intracellular signaling molecule activated by certain growth factors (Sundaresean et al., Science, 1995). An interest in aging and metabolism has led to three predominant research avenues in his laboratory. These include: autophagy in aging and age-related diseases; function and regulation of mitochondrial calcium levels, and substrate utilization as a determinant of cell fate.
Recent work from the Finkel lab has included the generation of mouse models that have increased or decreased autophagic flux. The lab has a particular interest in the potential role of autophagy within the vasculature. The lab is also interested in the process of mitophagy, a mechanism in which damaged or dysfunctional mitochondria are removed from the cell. In this regard, they have generated novel tools that allow mitophagy to be monitored in vivo. They have also generated various mouse models that lack components of the mitochondrial calcium uniporter (MCU) complex. This complex of proteins is located on the inner mitochondrial membrane and is responsible for the regulated entry of calcium ions into the mitochondrial matrix. Knockout animals in which various components of the MCU complex have been deleted are being explored in order to understand how mitochondrial calcium levels are regulated, and what role mitochondrial calcium plays in various physiological and pathophysiological conditions. Finally, the lab is interested in the role that substrate utilization plays in determining cellular fate. Cells can use a variety of metabolic substrates (e.g. glucose, fatty acids, etc.). Increasingly, evidence suggests that what fuel a cell uses, might help determine what the cell becomes or does. The basis for these observations is being explored using genetic models in which fatty acid oxidation is perturbed in a cell-type specific fashion.