ArticleJACC. Basic to translational science2025
Apolipoprotein A1 (CSL112) Increases Lecithin-Cholesterol Acyltransferase Levels in HDL Particles and Promotes Reverse Cholesterol Transport.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- The effect of oleic acid enriched diets on glucose and lipid metabolism: a systematic review and meta-analysis.Nutrition & metabolism · 2026Article
- A narrative review of impacts of apolipoproteins on atherosclerotic coronary plaques.NPJ cardiovascular health · 2026Review
- Targeting lymphatic dysfunction in atherosclerosis: a state-of-the-art review on potential therapies and future directions.Frontiers in cardiovascular medicine · 2026Review
- Advancing Secondary Prevention Post-Myocardial Infarction With CSL112.JACC. Basic to translational science · 2025Article
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Authors and funding
14 authors.
Funding
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Abstract
Although high-density lipoprotein (HDL) cholesterol is inversely correlated with cardiovascular risk, an emerging paradigm is focused on increasing reverse cholesterol transport (RCT) and HDL function via apolipoprotein A1 (ApoA1). The objective of this study was to investigate the effect of ApoA1 (CSL112) infusion on HDL protein composition, cholesterol esterification rate (CER), and cholesterol efflux capacity (CEC) in patients treated after acute myocardial infarction. CSL112 reduced levels of apolipoproteins A2, B, C, and E and serum amyloids A1 and A4, whereas ApoA1, ApoM, and lecithin-cholesterol acyltransferase were significantly elevated. Increased CEC, plasma HDL cholesterol levels, CER, and CEC also were observed in CSL112-treated patients.
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