Evidence map›Paper›PMID 34981790›Full record

ReviewThe Journal of clinical investigation2022

Addressing dyslipidemic risk beyond LDL-cholesterol.

Alan R Tall, David G Thomas, Ainara G Gonzalez-Cabodevilla, Ira J Goldberg

Open access · goldAbstract readReview
In one paragraph

Review in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
93citing papers in PubMed, 2 pooled it
19.2field-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

93 citing papers in PubMed, 2 syntheses or guidelines pooled it, 123 citations in OpenAlex.

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33 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Alan R TallDivision of Molecular Medicine, Department of Medicine, Columbia University, New York, New York, USA.
David G ThomasDivision of Molecular Medicine, Department of Medicine, Columbia University, New York, New York, USA.
Ainara G Gonzalez-CabodevillaDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University Grossman School of Medicine, New York, New York, USA.
Ira J GoldbergDivision of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University Grossman School of Medicine, New York, New York, USA.
Columbia University · USNew York University · US

Funding

Triglycerides, Diabetes and Cardiovascular DiseaseP01HL151328 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 2020 to 2026
$19.6M
Cholesterol efflux, CHIP and inflammasome activationR01HL107653 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ALAN richard TALL · 2011 to 2026
$7.7M
Pathways of Tissue Lipid UptakeR01HL045095 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABUMRAD, NADA A., GOLDBERG, IRA J · 1991 to 2024
$6.9M
EXTRACELLULAR REGULATION OF LIPOPROTEIN LIPASE ACTIVITYR37HL045095 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GOLDBERG, IRA J · 2000 to 2009
$4.6M
NHLBI NIH HHS P01 HL151328NHLBI NIH HHS R01 HL045095NHLBI NIH HHS R01 HL107653NHLBI NIH HHS R37 HL045095
6 · The paper itself

Abstract

Despite the success of LDL-lowering drugs in reducing cardiovascular disease (CVD), there remains a large burden of residual disease due in part to persistent dyslipidemia characterized by elevated levels of triglyceride-rich lipoproteins (TRLs) and reduced levels of HDL. This form of dyslipidemia is increasing globally as a result of the rising prevalence of obesity and metabolic syndrome. Accumulating evidence suggests that impaired hepatic clearance of cholesterol-rich TRL remnants leads to their accumulation in arteries, promoting foam cell formation and inflammation. Low levels of HDL may associate with reduced cholesterol efflux from foam cells, aggravating atherosclerosis. While fibrates and fish oils reduce TRL, they have not been uniformly successful in reducing CVD, and there is a large unmet need for new approaches to reduce remnants and CVD. Rare genetic variants that lower triglyceride levels via activation of lipolysis and associate with reduced CVD suggest new approaches to treating dyslipidemia. Apolipoprotein C3 (APOC3) and angiopoietin-like 3 (ANGPTL3) have emerged as targets for inhibition by antibody, antisense, or RNAi approaches. Inhibition of either molecule lowers TRL but respectively raises or lowers HDL levels. Large clinical trials of such agents in patients with high CVD risk and elevated levels of TRL will be required to demonstrate efficacy of these approaches.

Indexed as

AtherosclerosisCholesterol, LDLDyslipidemiasMetabolic SyndromeObesityAngiopoietin-Like Protein 3AnimalsApolipoprotein C-IIIFoam CellsGenetic VariationHumansLipoproteins, HDLAngiopoietin-Like Protein 3ANGPTL3 protein, humanAPOC3 protein, humanApolipoprotein C-IIICholesterol, LDLLipoproteins, HDL

Identifiers

PMID34981790
PMCPMC8718149
OpenAlexW4205596334

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.