A review on lecithin:cholesterol acyltransferase deficiency

Saeedi, Ramesh; Li, Min; Fröhlich, Jiří

doi:10.1016/j.clinbiochem.2014.08.014

Cited by 81 publications

(52 citation statements)

References 27 publications

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“…Exported from peripheral cells including endothelial cells, macrophages, smooth muscle cells, erythrocytes and platelets et al, FC was then accepted by lipid-free apolipoprotein (apo) AI to form immature preb-HDL [6]. Lecithin: cholesterol acyltransferase (LCAT) in the surface of HDL catalyzes the esterification of FC to form CE, which is then packed into the core of the HDL particles [7]. Only after the esterification of FC and translocation of CE, preb-HDL finally transforms into mature a-HDL.…”

Section: Discussionmentioning

confidence: 99%

Spontaneous and diet-aggravated hemolysis and its correction by probucol in SR-BI knockout mice with LDL-R deficiency

Liao

Gao

Wang

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

Spontaneous and diet-aggravated hemolysis and its correction by probucol in SR-BI knockout mice with LDL-R deficiency

Liao

Gao

Wang

et al. 2015

Biochemical and Biophysical Research Communications

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“…documented that in subjects with complete deficiency of LCAT, their increased atherosclerosis may be related to low LDL levels and not the lack of LCAT [18].…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, SAA impairs the antioxidant function of HDL [15], while the activity of HDL remodelling enzymes, such as lecithin cholesterol acyltransferase (LCAT), an enzyme that is responsible for the esterification of free cholesterol within HDL3 and thus its maturation to HDL2, is reduced by the presence of SAA [16]. However, the role of LCAT in the atherosclerotic process remains discordant [17], as reviewed [18].…”

Section: Introductionmentioning

confidence: 99%

Serum- and HDL3-serum amyloid A and HDL3-LCAT activity are influenced by increased CVD-burden

et al. 2016

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“…Whereas LCAT is clearly involved in the reverse cholesterol transport process and delivery of sterols to adrenal tissues, its role in atherosclerosis development is still debated (10 -16). Naturally occurring mutations in human apoA-I that are associated with low LCAT activities and low levels of HDL cholesterol have been extensively reviewed (13,17,18). These naturally occurring mutations, along with a variety of site-specific mutation and deletion studies, have suggested that multiple regions on apoA-I are important for LCAT interactions with HDL (6 -8, 19 -23).…”

mentioning

confidence: 99%

A Systematic Investigation of Structure/Function Requirements for the Apolipoprotein A-I/Lecithin Cholesterol Acyltransferase Interaction Loop of High-density Lipoprotein

Gu¹,

Wu²,

Huang³

et al. 2016

Journal of Biological Chemistry

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The interaction of lecithin-cholesterol acyltransferase (LCAT) with apolipoprotein A-I (apoA-I) plays a critical role in highdensity lipoprotein (HDL) maturation. We previously identified a highly solvent-exposed apoA-I loop domain (Leu 159 Apolipoprotein A-I (apoA-I), the major protein component of high-density lipoprotein (HDL), transports lipids and also serves as a protein scaffold for numerous HDL-associated protein interactions. The HDL particle is responsible for facilitating reverse cholesterol transport, a multistep process that removes cholesterol from peripheral tissues and ultimately from the body in feces. To promote its cholesterol carrier functions, apoA-I exists in multiple forms throughout the reverse cholesterol transport process. Initially, lipid-free or lipid-poor apoA-I becomes lipidated, generating the nascent HDL particle via the ATP-binding cassette transporter type 1 (ABCA1) 4 (1-4). Although capable of facilitating reverse cholesterol transport, subsequent maturation of the HDL particle into a cholesteryl ester-laden spherical particle substantially increases the capacity of the HDL particle to carry cholesterol cargo. Lecithin-cholesterol acyltransferase (LCAT) is the primary enzyme responsible for catalyzing the maturation of nascent HDL into spherical HDL by catalyzing esterification of free cholesterol (1). Fielding and colleagues (5) first showed that apoA-I within nascent HDL stimulates LCAT activity (5-7). The mechanism by which LCAT facilitates HDL maturation at the structural level is still unknown.-

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A review on lecithin:cholesterol acyltransferase deficiency

Cited by 81 publications

References 27 publications

Spontaneous and diet-aggravated hemolysis and its correction by probucol in SR-BI knockout mice with LDL-R deficiency

Spontaneous and diet-aggravated hemolysis and its correction by probucol in SR-BI knockout mice with LDL-R deficiency

Serum- and HDL3-serum amyloid A and HDL3-LCAT activity are influenced by increased CVD-burden

A Systematic Investigation of Structure/Function Requirements for the Apolipoprotein A-I/Lecithin Cholesterol Acyltransferase Interaction Loop of High-density Lipoprotein

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