Lecithin:cholesterol acyltransferase and vascular disease

Abstract

Evaluation of: Calabresi L, Baldassarre D, Castelnuovo S et al.: Functional lecithin:cholesterol acyltransferase is not required for efficient atheroprotection in humans. Circulation 120, 628–635 (2009). Lecithin:cholesterol acyltransferase (LCAT) is an HDL-associated enzyme responsible for esterifying free cholesterol to cholesteryl ester within the plasma compartment. Mutations in the LCAT gene can cause LCAT deficiency, a very rare metabolic disorder associated with two hypoalphalipoproteinemia syndromes; familial LCAT deficiency, characterized by complete lack of enzyme activity, and fish-eye disease, with a partially defective enzyme. As LCAT deficiency causes hypoalphalipoproteinemia, carriers should be at increased risk of coronary artery disease because of defective reverse cholesterol transport; however, owing to the relatively small number of cases available, this hypothesis has not been confirmed. Calabresi et al. take advantage of the availability of 13 LCAT-deficient families to investigate the extent of carotid preclinical atherosclerosis in these patients.

Keywords:

• atherosclerosis
• HDL
• lecithin:cholesterol acyltransferase