Evidence map›Paper›PMID 36367663›Full record

ReviewCurrent atherosclerosis reports2022

ANGPTL3 as a Drug Target in Hyperlipidemia and Atherosclerosis.

Farzahna Mohamed, Brett S Mansfield, Frederick J Raal

Open access · bronzeAbstract readReview
In one paragraph

Review in Current atherosclerosis reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
6.7field-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

32 citing papers in PubMed, 43 citations in OpenAlex.

  1. Association of circulating ANGPTL3 level with all-cause and cardiovascular mortality.International journal of cardiology. Cardiovascular risk and prevention · 2026
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  4. Leveraging Mendelian randomization to inform drug discovery and development for ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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  19. Simultaneously blocking ANGPTL3 and IL-1β for the treatment of atherosclerosis through lipid-lowering and anti-inflammation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  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

3 authors at 1 institution in 1 country.

Farzahna MohamedDepartment of Internal Medicine, Faculty of Health Sciences, Division of Endocrinology and Metabolism, University of the Witwatersrand, Johannesburg, South Africa.ORCID 0000-0001-5602-3621
Brett S MansfieldDepartment of Internal Medicine, Faculty of Health Sciences, Division of Endocrinology and Metabolism, University of the Witwatersrand, Johannesburg, South Africa.ORCID 0000-0002-8042-7041
Frederick J RaalDepartment of Internal Medicine, Faculty of Health Sciences, Division of Endocrinology and Metabolism, University of the Witwatersrand, Johannesburg, South Africa. frederick.raal@wits.ac.za.ORCID 0000-0002-9170-7938
University of the Witwatersrand · ZA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewElevated low-density lipoprotein cholesterol (LDL-C) and triglyceride-rich lipoproteins (TRLs) or remnants are important risk factors for the development of atherosclerotic cardiovascular disease (ASCVD). The ongoing challenge of not being able to achieve recommended LDL-C targets despite maximally tolerated lipid-lowering therapy (LLT) has led to the development of novel therapeutic agents including angiopoietin-like 3 (ANGPTL3) inhibitors. RECENT

findingsANGPTL3 is a glycoprotein produced by the liver that inhibits lipoprotein lipase and endothelial lipase. Data from genetic and clinical studies have shown that a lower ANGPTL3 level is associated with lower plasma LDL-C, triglyceride (TG), and other lipoproteins. Pharmacological inactivation of ANGPTL3 with the monoclonal antibody, evinacumab, results in a 50% reduction in LDL-C, even in patients with homozygous familial hypercholesterolemia (HoFH). The safe and effective targeted delivery of nucleic acid-based therapies will shape the future of the lipid arena. ANGPTL3 is a novel target in lipoprotein metabolism, targeting not only LDL-C via an LDL-receptor (LDLR) independent mechanism but also TRLs and carries a significant promise for further ASCVD risk reduction.

Indexed as

AtherosclerosisHyperlipidemiasMetabolic DiseasesAngiopoietin-Like Protein 3Angiopoietin-like ProteinsCholesterol, LDLHumansLipoproteinsTriglyceridesAngiopoietin-Like Protein 3Angiopoietin-like ProteinsANGPTL3 protein, humanCholesterol, LDLLipoproteinsTriglyceridesANGPTL3AtherosclerosisEndothelial lipaseLDL-CLipoprotein lipaseResidual cardiovascular riskTriglycerides

Identifiers

PMID36367663
PMCPMC9650658
OpenAlexW4308773486

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.