Evidence map›Paper›PMID 35873366›Full record

ReviewClinical pharmacology : advances and applications2022

Angiopoietin-Like Protein 3 (ANGPTL3) Inhibitors in the Management of Refractory Hypercholesterolemia.

Constantine E Kosmas, Maria D Bousvarou, Andreas Sourlas, Evangelia J Papakonstantinou, Edilberto Peña Genao, Rogers Echavarria Uceta, Eliscer Guzman

Open access · goldAbstract readReview
In one paragraph

Review in Clinical pharmacology : advances and applications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Trial
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  7. Article
  8. Novel RNA-Based Therapies in the Management of Dyslipidemias.International journal of molecular sciences · 2025
    Review
  9. Article
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  11. Review
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  20. Advances in Treatment of Dyslipidemia.International journal of molecular sciences · 2023
    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

7 authors at 2 institutions in 2 countries.

Constantine E KosmasDivision of Cardiology, Department of Medicine, Montefiore Medical Center, Bronx, NY, USA.
Maria D BousvarouSchool of Medicine, University of Crete, Heraklion, Greece.
Andreas SourlasSchool of Medicine, University of Crete, Heraklion, Greece.
Evangelia J PapakonstantinouGeneral Directorate of Public Health and Social Welfare, Athens, Attica Region, Greece.
Edilberto Peña GenaoCardiology Clinic, Cardiology Unlimited, PC, New York, NY, USA.
Rogers Echavarria UcetaCardiology Clinic, Cardiology Unlimited, PC, New York, NY, USA.
Eliscer GuzmanDivision of Cardiology, Department of Medicine, Montefiore Medical Center, Bronx, NY, USA.
Montefiore Medical Center · USUniversity of Crete · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiovascular disease (CVD) is the most common cause of death in a global scale and significantly depends on the elevated plasma levels of low-density lipoprotein cholesterol (LDL-C) and the subsequent formation of atherosclerotic plaques. While physicians have several LDL-C-lowering agents with diverse mechanisms of action, including statins, ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and inclisiran, angiopoietin-like protein 3 (ANGPTL3) inhibitors have recently emerged as a powerful addition in the armamentarium of lipid-lowering strategies, especially for patients with refractory hypercholesterolemia, as in the case of patients with homozygous familial hypercholesterolemia (HoFH). ANGPTL3 protein is a glycoprotein secreted by liver cells that is implicated in the metabolism of lipids along with other ANGPTL proteins. These proteins inhibit lipoprotein lipase (LPL) and endothelial lipase (EL) in tissues. Loss-of-function mutations affecting the gene encoding ANGPTL3 are linked with lower total cholesterol, LDL-C, and triglyceride (TG) levels. Evinacumab is a monoclonal antibody that targets, binds to, and pharmacologically inhibits ANGPTL3, which was recently approved by the United States Food and Drug Administration (FDA) as a complementary agent to other LDL-C lowering regimens for patients aged 12 or older with HoFH, based on clinical trial evidence that confirmed its safety and efficacy in those patients. Antisense oligonucleotides (ASOs) also represent an interesting class of agents that target and inhibit the mRNA derived from the transcription of

Indexed as

ANGPTL3 inhibitorscardiovascular diseaseevinacumabfamilial hypercholesterolemiaLDL-cholesterolLDL receptorsrefractory hypercholesterolemia

Identifiers

PMID35873366
PMCPMC9300746
OpenAlexW4285606737

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.