Purpose of review: Reverse cholesterol transport (RCT) is considered a significant component of the atheroprotective effects of HDL. Methods for quantifying flux through the RCT pathway have not been available until recently. There is a need to improve our understanding of HDL function, including the role of RCT in general and individual steps of RCT in particular, on atherosclerosis. This review highlights new information about cholesterol flux through the RCT pathway.
Recent findings: Recent clinical studies have demonstrated several important quantitative features of cholesterol fluxes in vivo, providing insight into variability and control of specific components of the RCT pathway. The findings illustrate the independent nature of individual steps in the RCT pathway and their apparently weak relationship to plasma HDL cholesterol levels. Nonclinical studies provide some mechanistic data re-enforcing the importance of apoB particles in RCT and role roles for serum albumin and erythrocytes in free cholesterol flux. These findings suggest that the HDL-centric view of RCT may need revision.
Summary: The constellation of known lipoproteins and other players involved in this pathway continues to increase. Further research, particularly in humans, is needed in order to understand which parts of the RCT pathway are most relevant to the pathophysiology and treatment of atherosclerosis.