Evidence map›Paper›PMID 34298929›Full record

ReviewInternational journal of molecular sciences2021

Angiopoietin-Like Protein 3 (ANGPTL3) Modulates Lipoprotein Metabolism and Dyslipidemia.

Pei-Yi Chen, Wan-Yun Gao, Je-Wen Liou, Ching-Yen Lin, Ming-Jiuan Wu, Jui-Hung Yen

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
8.2field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. In vivo base editing of Asgr1 reduces blood lipids in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Antibody-Based Therapeutics for Hypercholesterolemia.Biologics : targets & therapy · 2025
    Review
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

6 authors at 2 institutions in 1 country.

Pei-Yi ChenCenter of Medical Genetics, Hualien Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Hualien 970, Taiwan.ORCID 0000-0003-4270-7031
Wan-Yun GaoInstitute of Medical Sciences, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0001-7934-8402
Je-Wen LiouDepartment of Biochemistry, School of Medicine, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0002-6181-7263
Ching-Yen LinDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0002-8543-5059
Ming-Jiuan WuDepartment of Biotechnology, Chia Nan University of Pharmacy and Science, Tainan 717, Taiwan.ORCID 0000-0003-3327-828X
Jui-Hung YenDepartment of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan.ORCID 0000-0003-2551-350X
Tzu Chi University · TWChia Nan University of Pharmacy and Science · TW

Funding

Ministry of Science and Technology, Taiwan MOST 108-2320-B-320-002 -MY3
6 · The paper itself

Abstract

Dyslipidemia is characterized by increasing plasma levels of low-density lipoprotein-cholesterol (LDL-C), triglycerides (TGs) and TG-rich lipoproteins (TGRLs) and is a major risk factor for the development of atherosclerotic cardiovascular disorders (ASCVDs). It is important to understand the metabolic mechanisms underlying dyslipidemia to develop effective strategies against ASCVDs. Angiopoietin-like 3 (ANGPTL3), a member of the angiopoietin-like protein family exclusively synthesized in the liver, has been demonstrated to be a critical regulator of lipoprotein metabolism to inhibit lipoprotein lipase (LPL) activity. Genetic, biochemical, and clinical studies in animals and humans have shown that loss of function, inactivation, or downregulated expression of ANGPTL3 is associated with an obvious reduction in plasma levels of TGs, LDL-C, and high-density lipoprotein-cholesterol (HDL-C), atherosclerotic lesions, and the risk of cardiovascular events. Therefore, ANGPTL3 is considered an alternative target for lipid-lowering therapy. Emerging studies have focused on ANGPTL3 inhibition via antisense oligonucleotides (ASOs) and monoclonal antibody-based therapies, which have been carried out in mouse or monkey models and in human clinical studies for the management of dyslipidemia and ASCVDs. This review will summarize the current literature on the important role of ANGPTL3 in controlling lipoprotein metabolism and dyslipidemia, with an emphasis on anti-ANGPTL3 therapies as a potential strategy for the treatment of dyslipidemia and ASCVDs.

Indexed as

Angiopoietin-like ProteinsAnimalsAtherosclerosisCholesterol, HDLCholesterol, LDLDyslipidemiasHumansLipoproteinsTriglyceridesAngiopoietin-like ProteinsCholesterol, HDLCholesterol, LDLLipoproteinsTriglyceridesANGPTL3ASCVDsdyslipidemialipoprotein lipaseTG-rich lipoproteins

Identifiers

PMID34298929
PMCPMC8304944
OpenAlexW3178420100

What OpenQuestion 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 OpenQuestion graph.