ArticleArteriosclerosis, thrombosis, and vascular biology2012
Lipid oxidation in carriers of lecithin:cholesterol acyltransferase gene mutations.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- High-density lipoprotein: a biomarker and therapeutic target in sepsis.Critical care (London, England) · 2025Review
- Oxidized phospholipids in cardiovascular disease.Nature reviews. Cardiology · 2024Review
- Association of Plasma Vitamins and Carotenoids, DNA Methylation of LCAT, and Risk of Age-Related Macular Degeneration.Nutrients · 2023Article
- Effect of Short-Chain Fatty Acids and Polyunsaturated Fatty Acids on Metabolites in H460 Lung Cancer Cells.Molecules (Basel, Switzerland) · 2023Article
- Paraoxonase 1 and atherosclerosis.Frontiers in cardiovascular medicine · 2023Review
- HDL and Oxidation.Advances in experimental medicine and biology · 2022Article
- Good Cholesterol Gone Bad? HDL and COVID-19.International journal of molecular sciences · 2021Review
- Esterification of 4β-hydroxycholesterol and other oxysterols in human plasma occurs independently of LCAT.Journal of lipid research · 2020Article
- Antioxidative activity of high-density lipoprotein (HDL): Mechanistic insights into potential clinical benefit.BBA clinical · 2017Review
- Antioxidant properties of HDL.Frontiers in pharmacology · 2015Review
- High density lipoproteins and endothelial functions: mechanistic insights and alterations in cardiovascular disease.Journal of lipid research · 2013Review
- Review
- Feasibility of a plasma bioassay to assess oxidative protection of low-density lipoproteins by high-density lipoproteins.Journal of clinical lipidologyArticle
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveLecithin:cholesterol acyltransferase (LCAT) has been shown to play a role in the depletion of lipid oxidation products, but this has so far not been studied in humans. In this study, we investigated processes and parameters relevant to lipid oxidation in carriers of functional LCAT mutations. METHODS AND
resultsIn 4 carriers of 2 mutant LCAT alleles, 63 heterozygotes, and 63 family controls, we measured activities of LCAT, paraoxonase 1, and platelet-activating factor-acetylhydrolase; levels of lysophosphatidylcholine molecular species, arachidonic and linoleic acids, and their oxidized derivatives; immunodetectable oxidized phospholipids on apolipoprotein (apo) B-containing and apo(a)-containing lipoproteins; IgM and IgG autoantibodies to malondialdehyde-low-density lipoprotein and IgG and IgM apoB-immune complexes; and the antioxidant capacity of high-density lipoprotein (HDL). In individuals with LCAT mutations, plasma LCAT activity, HDL cholesterol, apoA-I, arachidonic acid, and its oxidized derivatives, oxidized phospholipids on apo(a)-containing lipoproteins, HDL-associated platelet-activating factor-acetylhydrolase activity, and the antioxidative capacity of HDL were gene-dose-dependently decreased. Oxidized phospholipids on apoB-containing lipoproteins was increased in heterozygotes (17%; P<0.001) but not in carriers of 2 defective LCAT alleles.
conclusionsCarriers of LCAT mutations present with significant reductions in LCAT activity, HDL cholesterol, apoA-I, platelet-activating factor-acetylhydrolase activity, and antioxidative potential of HDL, but this is not associated with parameters of increased lipid peroxidation; we did not observe significant changes in the oxidation products of arachidonic acid and linoleic acid, immunoreactive oxidized phospholipids on apo(a)-containing lipoproteins, and IgM and IgG autoantibodies against malondialdehyde-low-density lipoprotein. These data indicate that plasma LCAT activity, HDL-associated platelet-activating factor-acetylhydrolase activity, and HDL cholesterol may not influence the levels of plasma lipid oxidation products.
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