High density lipoproteins (HDL) are considered the “good cholesterol” largely because of their role in the reverse cholesterol transport pathway. In this pathway, cholesterol is transported via HDL particles to the liver for excretion in the bile or to steroidogenic tissues for steroid hormone synthesis. My projects focus on understanding a vital interaction in this pathway: HDL with its primary receptor, Scavenger receptor class B type I (SR-BI). We are particularly interested in how mutations or oxidative stress to the receptor or ligand can impact the ability of SR-BI interact with HDL and promote HDL-cholesterol ester uptake. Our lab studies this interaction with the goal of finding mechanisms to lower whole body cholesterol and reduce the risk of cardiovascular disease.