Cardiovascular disease (CVD) is the leading cause of death and disability worldwide. Vascular remodeling—alterations in the structure of blood vessels—plays a key role during embryogenesis and in causing the vessel damage that occurs in atherosclerosis and other manifestations of CVD.

Vascular smooth muscle cells are the main drivers of vascular remodeling, but the mechanisms underlying smooth muscle cell activities—in particular, the roles played by mitochondria and metabolism—are not well understood. Studies conducted in the laboratory of Nicholas Sibinga, M.D., indicate that mitochondrial complex 1—the largest enzyme complex of the mitochondrial respiratory chain—regulates vascular smooth muscle cell behavior.

He has received a four-year, $2 million NIH grant to study mitochondria-mediated regulation of vascular wall function during embryogenesis and in mouse models of vascular disease in adulthood. His lab will use genetically modified mice and pharmacological strategies to characterize how mitochondrial function impinges on the vasculature in health and disease. The goal of the research is to identify vascular remodeling targets that are susceptible to drug intervention, resulting in enhanced health, increased lifespan, and reduced vascular disease disability. Dr. Sibinga is professor of medicine and of developmental and molecular biology at Einstein and a cardiologist at Montefiore. (1R01HL149921-01)