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Toren Finkel, M.D., Ph.D., joined the National Heart, Lung, and Blood Institute (NHLBI) in 1992 as Investigator in the Cardiology Branch. He is currently Chief of the Center for Molecular Medicine in the Institute's Division of Intramural Research.
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 when activated by certain growth factors. An interest in aging and metabolism has led to four related research avenues in his laboratory: (1) oxidative homeostasis in stem cell biology, (2) the use of cellular senescence as a model for aging, (3) autophagy in aging and age-related diseases, and (4) interrogating pathways identified in lower organisms to understand their role in mammalian aging.
Dr. Finkel received his M.D. from Harvard Medical School, Boston, MA in 1986. That same year, he received his Ph.D. in Biophysics from the Harvard University School of Arts and Sciences. He graduated summa cum laude in 1979 with a B.S. in Physics from the University of Maryland, College Park. Dr. Finkel pursued a Fellowship in Cardiology at the Johns Hopkins University Hospital from 1989-1992. He conducted his Internship and Residency in Internal Medicine at Massachusetts General Hospital from 1986-1987 and 1987-1989, respectively.
Dr. Finkel is the author or coauthor of over 80 publications. He has edited one book and is Editor-in-Chief of Drug Discovery Today-Disease Mechanisms. Dr. Finkel also is the Associate Editor of Circulation Research and is on the editorial boards of several peer-reviewed journals.
February 22, 2013
: Cell Press
Cell Press webinar: signaling and mitochondria
co-presented by Toren Finkel, M.D., Ph.D., Center for Molecular Medicine
Recent years have witnessed a growing excitement in the field of mitochondrial biology with a dramatic increase in our appreciation of the diversity and complexity of mitochondrial function. Rather than simply acting as isolated energy-generating organelles, as once thought, we now know that these organelles form a dynamic network that is subject to continuous remodeling and is integrated into cellular signaling pathways. This webinar will focus on recent developments in signaling at mitochondria, specifically the role of oxidative stress signalling in metabolism, the regulation of mitochondrial calcium dynamics, and the contribution of the ubiquitin-proteasome system in modulating mitochondrial dynamics.
December 14, 2012
The NAD-dependent deacetylase SIRT2 is required for programmed necrosis
co-authored by Toren Finkel, Elizabeth Murphy, and Michael Sack
Although initially viewed as unregulated, increasing evidence suggests that cellular necrosis often proceeds through a specific molecular program. In particular, death ligands such as tumour necrosis factor (TNF)-α activate necrosis by stimulating the formation of a complex containing receptor-interacting protein 1 (RIP1) and receptor-interacting protein 3 (RIP3). Relatively little is known regarding how this complex formation is regulated. Here, we show that the NAD-dependent deacetylase SIRT2 binds constitutively to RIP3 and that deletion or knockdown of SIRT2 prevents formation of the RIP1–RIP3 complex in mice.