Cited by 232Lipid metabolism and disordersLipid metabolism and biosynthesisLipoproteins and Cardiovascular Health

Apolipoprotein C-II: new findings related to genetics, biochemistry, and role in triglyceride metabolism

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Wolska, Anna, Dunbar, Richard L., Freeman, Lita A., Ueda, Masako, Amar, Marcelo J., Sviridov, Denis O., Remaley, Alan T.·2017·Atherosclerosis

Abstract

Apolipoprotein C-II (apoC-II) is a small exchangeable apolipoprotein found on triglyceride-rich lipoproteins (TRL), such as chylomicrons (CM) and very low-density lipoproteins (VLDL), and on high-density lipoproteins (HDL), particularly during fasting. ApoC-II plays a critical role in TRL metabolism by acting as a cofactor of lipoprotein lipase (LPL), the main enzyme that hydrolyses plasma triglycerides (TG) on TRL. Here, we present an overview of the role of apoC-II in TG metabolism, emphasizing recent novel findings regarding its transcriptional regulation and biochemistry. We also review the 24 genetic mutations in the APOC2 gene reported to date that cause hypertriglyceridemia (HTG). Finally, we describe the clinical presentation of apoC-II deficiency and assess the current therapeutic approaches, as well as potential novel emerging therapies.

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Crossref · 10.1016/j.atherosclerosis.2017.10.025

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  • Apoc2 is implicated in metabolism of triglyceride-rich lipoproteins by acting as a cofactor of lipoprotein lipase, the main enzyme that hydrolyses plasma triglycerides on TRL.

    “For instance, there was a negative relationship between the relative abundance of two Lachnospiraceae ASVs (ASV0048 & ASV0056) and methylation at a DMR nearby apolipoprotein C2, a gene implicated in metabolism of triglyceride-rich lipoproteins (TRLs) by acting as a cofactor of lipoprotein lipase (LPL), the main enzyme that hydrolyses plasma triglycerides on TRL59.”
  • Apo C-II is a cofactor for LPL.

    “Apo C-II is a cofactor for LPL91,92”

    From Clinical review on triglycerides (2020) · cites this paper as [92]

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2 retracted

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1 of the 125 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. [102]Herink M I M Medication Induced Changes in Lipid and Lipoproteins De Groot LJ C G Dungan K Endotext (Internet) MDText.com, Inc. South Dartmouth (MA) Updated 2015 Jul 27, https://www.ncbi.nlm.nih.gov/books/NBK326739/

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Authors
Wolska, A., Dunbar, R. L., Freeman, L. A., Ueda, M., Amar, M. J., Sviridov, D. O., & Remaley, A. T.
Affiliations
  • National Institutes of Health (US)
  • Philadelphia VA Medical Center (US)
  • University of Pennsylvania (US)
Corresponding author
Wolska, Anna
Venue
Atherosclerosis
Publisher
Elsevier BV
Published
2017-12
Volume
267
Pages
49-60
ISSN
0021-9150 (ISSN-L)
OpenAlex
W2767128978
Cited by
231
References
125
Citations by year
2026: 18 · 2025: 28 · 2024: 20 · 2023: 35 · 2022: 34 · 2021: 44 · 2020: 25 · 2019: 15 · 2018: 11
FWCI
1.97
Type
journal article
Language
en
Open access
Locations
  • Atherosclerosis (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • National Heart, Lung, and Blood Institute (ZIAHL006095)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Keywords
apolipoprotein C-II, triglyceride metabolism, triglyceride-rich lipoproteins, chylomicrons, VLDL, high-density lipoprotein, hypertriglyceridemia, transcriptional regulation, treatment options
MeSH terms
Animals, Chylomicrons, Gene Expression Regulation, Multigene Family, Humans, Hydrolysis, Intestinal Mucosa, Lipolysis, Lipoprotein Lipase, Lipoproteins, Lipoproteins, HDL, Lipoproteins, VLDL, Liver, Macrophages, Mutation, Transcription, Genetic, Triglycerides, Mice, Rats, Apolipoprotein C-II

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