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Genetic lecithin:cholesterol acyltransferase deficiency and cardiovascular disease.

Abstract
The lecithin:cholesterol acyltransferase (LCAT) enzyme is responsible for the synthesis of cholesteryl esters in human plasma and plays a critical role in high density lipoprotein (HDL) metabolism. Genetic LCAT deficiency is a rare metabolic disorder characterized by low HDL cholesterol levels. This paper reviews the genetic and biochemical features of LCAT deficiency, highlighting the absence of enhanced preclinical atherosclerosis in carriers, despite the remarkably low HDL cholesterol.
AuthorsLaura Calabresi, Sara Simonelli, Monica Gomaraschi, Guido Franceschini
JournalAtherosclerosis (Atherosclerosis) Vol. 222 Issue 2 Pg. 299-306 (Jun 2012) ISSN: 1879-1484 [Electronic] Ireland
PMID22189200 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
CopyrightCopyright © 2011 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • Cholesterol Esters
  • Cholesterol, HDL
  • Phosphatidylcholine-Sterol O-Acyltransferase
Topics
  • Adult
  • Animals
  • Cardiovascular Diseases (blood, enzymology, etiology, genetics)
  • Cholesterol Esters (blood)
  • Cholesterol, HDL (blood)
  • Female
  • Genetic Predisposition to Disease
  • Humans
  • Hypoalphalipoproteinemias (blood, enzymology, etiology, genetics)
  • Lecithin Cholesterol Acyltransferase Deficiency (blood, complications, enzymology, genetics)
  • Male
  • Middle Aged
  • Mutation
  • Phenotype
  • Phosphatidylcholine-Sterol O-Acyltransferase (genetics)
  • Risk Assessment
  • Risk Factors

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