NIH awards grant for vascular decalcification

New York Institute of Technology secures $1.8M grant to investigate vascular decalcification

January 27, 2021
DDN Staff

OLD WESTBURY, NY—A research team led by Dr. Olga V. Savinova, assistant professor of biomedical sciences in the College of Osteopathic Medicine at the New York Institute of Technology, has secured a grant from the National Institutes of Health (NIH)’s National Heart, Lung, and Blood Institute. The $1.8 million five-year grant — which includes a first-year award of $342,675 — will support research to improve the understanding of atherosclerosis. It also has the potential to deliver a new treatment for heart disease.

Researchers believe that atherosclerosis is a risk factor in predicting heart disease-related illness and death. Vascular calcification is a buildup of calcium salts in blood vessel tissue. This buildup is considered a hallmark of atherosclerosis, but it’s unclear whether calcification is the cause of atherosclerosis, or merely a byproduct. If vascular calcification is a risk factor, treatments targeting calcification might be able to prevent heart disease cases and fatalities.

“Our overarching goal is to gain a better understanding of how calcification impacts the onset, progression, and treatment of atherosclerosis,” explained Savinova, who also received an NIH grant to examine vascular calcification in chronic kidney disease in 2018. “We believe calcification is a risk factor for atherosclerosis, and one that can be corrected. By inhibiting vascular calcification caused by overactive phosphatase, we may be able to provide a therapy for atherosclerosis.” 

The team plans to find out whether vascular calcification contributes to the development of atherosclerosis — and if so, whether a decalcification treatment would be able to correct and prevent it. Computational models will map the blood flow impact of increased calcification in mice with high lipid levels. After administering an inhibitor to mitigate excess enzyme activity, the team will monitor for reductions in arterial stress. If this approach is successful, it could also prevent harmful changes around the aortic valve, which is critical to proper circulation. 

Savinova’s team has collected data that suggests phosphatase is responsible for vascular calcification. Their research shows that when a surplus of phosphatase exists in combination with high lipid levels, lipids are retained in the blood vessels, and accelerate vessel hardening. If the overactive gene responsible for the surplus can be “turned down,” preventing its ability to cause calcification, atherosclerosis might be treatable. 

Other New York Institute of Technology contributors include Dr. Dorinamaria Carka, assistant professor of mechanical engineering, who will lead computer simulations studies on blood flow dynamics; Dr. Brian Beatty, associate professor of anatomy; and Dr. Maria Plummer, pathologist and associate professor of clinical specialties. Dr. Jose Luis Millan, human genetics professor at the Sanford Burnham Prebys Medical Discovery Institute, will also be a contributor.

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