Evidence mapPaperPMID 37972731Full record

ReviewJournal of lipid research2024

Apolipoprotein C3: form begets function.

Karin E Bornfeldt

Open access · goldAbstract readReview
In one paragraph

Review in Journal of lipid research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 3 pooled it
11.7field-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

25 citing papers in PubMed, 3 syntheses or guidelines pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Review
  5. Article
  6. Current and Emerging Pharmacological Therapies for Hypertriglyceridemia.International journal of molecular sciences · 2026
    Review
  7. Article
  8. Article
  9. Rodent Models for Atherosclerosis.International journal of molecular sciences · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. 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

1 author at 1 institution in 1 country.

Karin E BornfeldtDivision of Metabolism, Endocrinology and Nutrition, Department of Medicine, UW Medicine Diabetes Institute and Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA. Electronic address: bornf@uw.edu.
University of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · 1986 to 2025
$12.6M
Triglycerides, Diabetes and Cardiovascular DiseaseP01HL151328 · UNIVERSITY OF WASHINGTON · 2025 to 2025
$2.6M
Apolipoprotein C3-loading of apolipoprotein B100 lipoproteins and cardiovascular disease in patients with type 1 diabetesR01HL161829 · NHLBI · UNIVERSITY OF WASHINGTON · 2023 to 2025
$2.5M
Structural basis for cardioprotective HDLR01HL149685 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt, JAY W HEINECKE · 2022 to 2023
$1.4M
Identifying new strategies for prevention of cardiovascular complications of diabetesR35HL150754 · UNIVERSITY OF WASHINGTON · 2025 to 2025
$1.1M
NHLBI NIH HHS P01 HL151328NHLBI NIH HHS R01 HL149685NHLBI NIH HHS R01 HL161829NHLBI NIH HHS R35 HL150754NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

Increased circulating levels of apolipoprotein C3 (APOC3) predict cardiovascular disease (CVD) risk in humans, and APOC3 promotes atherosclerosis in mouse models. APOC3's mechanism of action is due in large part to its ability to slow the clearance of triglyceride-rich lipoproteins (TRLs) and their remnants when APOC3 is carried by these lipoproteins. However, different pools and forms of APOC3 exert distinct biological effects or associations with atherogenic processes. Thus, lipid-free APOC3 induces inflammasome activation in monocytes whereas lipid particle-bound APOC3 does not. APOC3-enriched LDL binds better to the vascular glycosaminoglycan biglycan than does LDL depleted of APOC3. Patterns of APOC3 glycoforms predict CVD risk differently. The function of APOC3 bound to HDL is largely unknown. There is still much to learn about the mechanisms of action of different forms and pools of APOC3 in atherosclerosis and CVD, and whether APOC3 inhibition would prevent CVD risk in patients on LDL-cholesterol lowering medications.

Indexed as

AtherosclerosisLipoproteinsAnimalsApolipoprotein C-IIIHumansMiceTriglyceridesApolipoprotein C-IIILipoproteinsTriglyceridesApolipoproteinsAtherosclerosisInflammationLDLTriglyceridesVLDL

Identifiers

PMID37972731
PMCPMC10805671
OpenAlexW4388662938

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.