Abnormal mineral deposition in the soft tissues (calcification) can be seen in some life-threatening diseases. Mineral accumulation in the blood vessels is a common example of soft tissue calcification. Although vascular calcification is seen in aging population and considered as a risk factor for many vascular diseases the mechanisms that regulate this process is poorly understood. A better understanding of the determinants of this complex process will identify novel therapeutic targets to prevent and manage vascular calcification in humans.
My objective for the current project is to analyze the vascular calcification trait in a mouse model that lacks a potent anti-mineralization protein. In this model, absence of the anti-mineralization protein leads to massive deposition of minerals in the arterial walls. I will investigate the cell behavior in the calcified arteries of this model and determine how protein breakdown in these arteries affects the severity of the disease. I will treat this model with a pharmacologic agent to inhibit protein breakdown with a goal to prevent vascular calcification.