Evidence map›Paper›PMID 38039351›Full record

ReviewCardiovascular research2024

Exploring apolipoprotein C-III: pathophysiological and pharmacological relevance.

Chris J Packard, Angela Pirillo, Sotirios Tsimikas, Brian A Ference, Alberico L Catapano

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
14.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Article
  3. Atherogenic apolipoprotein C-III may not be as bad as we thought.Journal of thrombosis and haemostasis : JTH · 2026
    Article
  4. Review
  5. Current and Emerging Pharmacological Therapies for Hypertriglyceridemia.International journal of molecular sciences · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Oxidised Apolipoprotein Peptidome Characterises Metabolic Dysfunction-Associated Steatotic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 5 institutions in 4 countries.

Chris J PackardInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.ORCID 0000-0002-2386-9927
Angela PirilloCenter for the Study of Atherosclerosis, E. Bassini Hospital, Milan, Italy.ORCID 0000-0002-2948-6257
Sotirios TsimikasDivision of Cardiovascular Medicine, Sulpizio Cardiovascular Center, University of California San Diego, La Jolla, CA, USA.
Brian A FerenceCentre for Naturally Randomized Trials, University of Cambridge, Cambridge, UK.
Alberico L CatapanoCenter for the Study of Dyslipidaemias, IRCCS MultiMedica, Sesto S. Giovanni, 20099 Milan, Italy.ORCID 0000-0002-7593-2094
MultiMedica · ITUniversity of California San Diego · USUniversity of Cambridge · GBUniversity of Glasgow · GBUniversity of Milan · IT

Funding

Translating Lp(a) biology to clinical applicationsR01HL159156 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SOTIRIOS TSIMIKAS · 2022 to 2026
$3.3M
NHLBI NIH HHS R01 HL159156
6 · The paper itself

Abstract

The availability of pharmacological approaches able to effectively reduce circulating LDL cholesterol (LDL-C) has led to a substantial reduction in the risk of atherosclerosis-related cardiovascular disease (CVD). However, a residual cardiovascular (CV) risk persists in treated individuals with optimal levels of LDL-C. Additional risk factors beyond LDL-C are involved, and among these, elevated levels of triglycerides (TGs) and TG-rich lipoproteins are causally associated with an increased CV risk. Apolipoprotein C-III (apoC-III) is a key regulator of TG metabolism and hence circulating levels through several mechanisms including the inhibition of lipoprotein lipase activity and alterations in the affinity of apoC-III-containing lipoproteins for both the hepatic receptors involved in their removal and extracellular matrix in the arterial wall. Genetic studies have clarified the role of apoC-III in humans, establishing a causal link with CVD and showing that loss-of-function mutations in the APOC3 gene are associated with reduced TG levels and reduced risk of coronary heart disease. Currently available hypolipidaemic drugs can reduce TG levels, although to a limited extent. Substantial reductions in TG levels can be obtained with new drugs that target specifically apoC-III; these include two antisense oligonucleotides, one small interfering RNA and an antibody.

Indexed as

AtherosclerosisCoronary DiseaseApolipoprotein C-IIICholesterol, LDLHumansLipoproteinsTriglyceridesAPOC3 protein, humanApolipoprotein C-IIICholesterol, LDLLipoproteinsTriglyceridesApolipoprotein C-IIICardiovascular diseaseGeneticsTriglyceride-rich lipoproteinsTriglycerides

Identifiers

PMID38039351
PMCPMC11484501
OpenAlexW4389220157

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.