University of Michigan
United States of America
David J. Pinsky, is the division chief of Cardiovascular Medicine at the University of Michigan, as well as the scientific director of the U-M Cardiovascular Center. Prior to joining U-M in March 2003, Pinsky was director of research for the Cardiovascular Disease Training Program at Columbia Presbyterian Medical Center in New York and associate professor of Medicine at Columbia University College of Physicians & Surgeons. He served at Columbia University from 1992-2003. He earned his medical degree from Ohio State University and performed his medicine residency, as well as his research fellowship in heart failure at Mount Sinai Hospital in New York. He also performed research fellowships in cardiology and vascular biology at Columbia. As a result of his groundbreaking research, Dr. Pinsky has earned a reputation as one of the country's foremost experts in understanding the relationship between blood flow and heart and brain diseases. His research efforts have earned him numerous grants and awards, including the American Heart Association Melvin Marcus Young Investigator Award in cardiovascular physiology and the AHA Established Investigator Award.
Dr. Pinsky’s work focuses on mechanisms driving hypoxic/ischemic modulation of the vascular phenotype. His early work showed that restoring vascular homeostasis in preserved organs, through repletion of deficient second nucleotide messengers, prevents primary graft failure. This led to the first direct in vivo measurements of nitric oxide (NO), by Dr. Pinsky and colleagues, and their discovery that NO synthesis is mechanically transduced in the beating heart. His group first showed that carbon monoxide (CO) was not simply a toxic byproduct of heme catabolism, but a cytoprotectant under ischemic stress. He subsequently elucidated the transcriptional signaling mechanism underlying CO’s cytoprotective effects, and showed that inhaled CO not only restores vascular homeostasis but mitigates chronic rejection. Other work includes his group's recent discovery of a new HIF-1a-independent hypoxia-response motif driving ischemic upregulation of coagulant genes, and the potent endogenous protective role for ENTDPase 1 (CD39, which catalyzes the terminal phosphohydrolysis of adenine nucleotides under ischemic conditions such as stroke). Overall, his work has led to new insights into mechanisms driving maladaptive responses of the vasculature to hypoxia or ischemia, and means for their mitigation. The laboratory is a dynamic environment which focuses on translational vascular medicine, so that the molecular mechanisms being studied are made relevant to disease models such as stroke, myocardial infarction, and heart and lung transplantation. Most of the experimental models seek to elucidate the role of native genes (CD39, CD73, Egr-1, heme oxyygenase, eicosanoids) and their products/reactions in maintaining vascular homeostasis or restoring homeostasis after an ischemic insult. Experimental methodologies range from the molecular (cloning, promoter-reporter analyses, gene-targetting, gene-silencing, etc), to the cellular (cell culture, transfection, hypoxia, CO exposure), to the organismal (gene mutant mice, heart transplantation, lung transplantation, stroke, myocardial infarction). Trainees are expected to participate actively in experimental design and execution, manuscript and grant preparation, and other interactive research activities.