Genetics of Vascular Smooth Muscle Cells May Play Key Role in Coronary Artery Disease (CAD); Study Identifies One Gene (MIA3) with Protective Effect in CAD Plaque Formation

Researchers at the University of Virginia (UVA) have shed light on how our genes affect our risk for coronary artery disease, the most common form of heart disease. In addition to identifying gene variants that influence risk, they found that one gene in particular (MIA3) appears to have a protective effect. Doctors may be able to use the findings to identify people at high risk and to develop better treatments and preventative interventions. "Current drugs for coronary artery disease treat the risk factors, such as cholesterol or hypertension," said researcher Mete Civelek (photo), PhD, of UVA's Department of Biomedical Engineering and UVA's Center for Public Health Genomics. "Our studies used a genetic approach to identify the mechanisms in the wall of the blood vessels where the disease actually develops." Heart disease is the most common cause of death in the United States, killing one person every 36 seconds. About 18.2 million Americans have the form known as coronary artery disease, or CAD. The federal Centers for Disease Control and Prevention (CDC) estimates that more than 350,000 Americans died from CAD in 2017. Scientists have known that our risk for CAD is affected by diet, smoking, exercise, and other factors, including family history, but the role of our genes remains poorly understood. To better understand this, Dr. Civelek and his colleagues began by examining cells from 151 ethnically diverse heart donors. These cells, called vascular smooth muscle cells, can prove either beneficial or harmful in the buildup of fatty plaques inside our blood vessels. That buildup, known as atherosclerosis, causes CAD. The researchers examined the smooth muscle cells for 12 different characteristics that influence the stability of the plaque patches.
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