A New York Institute of Technology research team led by Olga V. Savinova, Ph.D., assistant professor of biomedical sciences at the New York Institute of Technology College of Osteopathic Medicine (NYITCOM), was awarded a five-year grant from the National Institutes of Health (NIH) National Heart, Lung, and Blood Institute. The $ 1.8 million grant, which includes a first-year scholarship of $ 342,675, will support research aimed at improving understanding of atherosclerosis (hardening of the arteries) and providing a new treatment for heart disease.
According to the Centers for Disease Control and Prevention, more than 30 million American adults have been diagnosed with heart disease, which also causes one in four deaths. Researchers have long believed that atherosclerosis is a risk factor in predicting heart disease and death. The build-up of calcium salts in the tissues of blood vessels, known as vascular calcification, is considered a hallmark of atherosclerosis, but it is not known whether calcification causes atherosclerosis or is simply an under- product. While this is a risk factor, treatments targeting calcification can prevent millions of future cases of heart disease and death.
The team will use mouse and computer models to determine whether vascular calcification contributes to the development of atherosclerosis and, if so, whether decalcification treatment can correct and prevent it.
“Our primary goal is to better understand how calcification affects the onset, progression and treatment of atherosclerosis.“said Savinova, who also received a 2018 NIH grant to examine vascular calcification in chronic kidney disease.”We believe that calcification is a risk factor for atherosclerosis and one that can be corrected. By inhibiting vascular calcification caused by overactive phosphatase, we might be able to provide therapy for atherosclerosis. “
Savinova’s team collected data suggesting that the enzyme phosphatase is responsible for vascular calcification. Their research shows that when an excess of phosphatase exists in combination with high levels of lipids, the lipids are retained in the blood vessels, accelerating the hardening of the vessels. Therefore, if the hyperactive gene responsible for the surplus can be “turned down”, preventing its ability to cause calcification, atherosclerosis can also be treated.
Computer models will map the impact on blood flow of increased calcification in mice with high lipid levels. After administering an inhibitor to alleviate excess enzyme activity, the team will monitor the reduction in arterial stress. If their approach is successful, it could also prevent harmful changes in the area of the heart containing the aortic valve, which is essential for good circulation.
Other New York Tech contributors include Dorinamaria Carka, Ph.D., assistant professor of mechanical engineering, who will lead computer simulation studies on the dynamics of blood flow, Brian Beatty, Ph.D., associate professor of anatomy , and Maria Plummer, MD, pathologist and associate professor of clinical specialties. Jose Luis Millan, Ph.D., professor of human genetics at the Sanford Burnham Prebys Medical Discovery Institute, is also involved.
The NIH, part of the US Department of Health and Human Services, is the world’s largest biomedical research agency. The grant was supported by the NIH National Heart, Lung, and Blood Institute under the award number R01HL149864. The contents are the sole responsibility of the authors and do not necessarily represent the official views of the NIH.