PHILADELPHIA -- The biggest risks for cardiovascular disease are smoking and poor diet. However, different people are more susceptible to heart disease based on very slight differences in their genes, called variants. While there have been many studies that have linked variants to cardiovascular traits, it’s unclear whether these variants have functional consequences, like altered gene or protein expression. In a new study from the Cardeza Foundation for Hematologic Research at Thomas Jefferson University, researchers have discovered two slight gene variations that may modulate the behavior of platelet cells, and subsequently affect the risk of developing cardiovascular disease.
Normally, when platelets become activated, they stick together and clot wounds to stop bleeding. In disease, platelets can aggregate in response to triggers like unhealthy fats, and contribute to plaque formation in diseases like atherosclerosis. “Platelet numbers and volume are regulated by the expression of certain genes,” says Leonard Edelstein, PhD, research assistant professor and senior author of the study. “If there’s more of that gene, there are more platelets and a tendency to clot more.” CD36 is one such gene that regulates platelet levels and activation.