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Toren Finkel, M.D., Ph.D.
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Toren Finkel, M.D., Ph.D.
Biography
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.
Dr. Finkel In the News
December 14, 2012
: Nature
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.
February 12, 2003
NHLBI Study Finds Possible New Indicator of Heart Disease Risk
Levels of a type of adult stem cell in the bloodstream may indicate a person's risk of developing cardiovascular disease, according to a study supported by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health in Bethesda, MD.
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