Lecithin: cholesterol acyltransferase and vascular disease

Giuseppe Danilo Norata, Alberico Luigi Catapano

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)13-15
Number of pages3
JournalFuture Lipidology
Volume5
Issue number1
DOIs
Publication statusPublished - 2010

Keywords

  • Atherosclerosis
  • HDL
  • Lecithin:cholesterol acyltransferase

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Endocrinology, Diabetes and Metabolism

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