Evidence map›Paper›PMID 21986251›Full record

ReviewBiochimica et biophysica acta2012

The effect of hepatic lipase on coronary artery disease in humans is influenced by the underlying lipoprotein phenotype.

John D Brunzell, Alberto Zambon, Samir S Deeb

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
2.5field-weighted citation impact, top 11% 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, 2 syntheses or guidelines pooled it, 59 citations in OpenAlex.

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  9. Atherosclerosis and Its Related Laboratory Biomarkers.International journal of molecular sciences · 2023
    Review
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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 2 institutions in 1 country.

John D BrunzellUniversity of Washington, Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, Box 356426, 1959 NE Pacific Avenue, Seattle, Washington 98195, USA. brunzell@uw.edu
Alberto Zambon
Samir S Deeb
University of Washington · USUniversity of Washington Medical Center · US

Funding

Serum Amyloid and Inflammation in AtherogenesisP01HL030086 · NHLBI · UNIVERSITY OF WASHINGTON · PI JARVIK, GAIL PAIRITZ · 1985 to 2009
$14.7M
GENETICS &REGULATION OF HEPATIC LIPASER01HL064322 · NHLBI · UNIVERSITY OF WASHINGTON · PI DEEB, SAMIR S · 1999 to 2005
$1.9M
NHLBI NIH HHS HL 30086NHLBI NIH HHS HL 64322NHLBI NIH HHS P01 HL030086NHLBI NIH HHS R01 HL064322
6 · The paper itself

Abstract

Increased or decreased hepatic lipase (HL) activity has been associated with coronary artery disease (CAD). This is consistent with the findings that gene variants that influence HL activity were associated with increased CAD risk in some population studies but not in others. In this review, we will explain the conditions that influence the effects of HL on CAD. Increased HL is associated with smaller and denser LDL (sdLDL) and HDL (HDL(3)) particles, while decreased HL is associated with larger and more buoyant LDL and HDL particles. The effect of HL activity on CAD risk is dependent on the underlying lipoprotein phenotype or disorder. Central obesity with hypertriglyceridemia (HTG) is associated with high HL activity that leads to the formation of sdLDL that is pro-atherogenic. In the absence of HTG, where large buoyant cholesteryl ester-enriched LDL is prominent, elevation of HL does not raise the risk for CAD. In HTG patients, drug therapy that decreases HL activity selectively decreases sdLDL particles, an anti-atherogenic effect. Drug therapy that raises HDL(2) cholesterol has not decreased the risk for CAD. In trials where inhibition of cholesterol ester transfer protein (CETP) or HL occurs, the increase in HDL(2) most likely is due to inhibition of catabolism of HDL(2) and impairment of reverse cholesterol transport (RCT). In patients with isolated hypercholesterolemia, but with normal triglyceride levels and big-buoyant LDL particles, an increase in HL activity is beneficial; possibly because it increases RCT. Drugs that lower HL activity might decrease the risk for CAD only in hypertriglyceridemic patients with sdLDL by selectively clearing sdLDL particles from plasma, which would override the potentially pro-atherogenic effect on RCT. This article is part of a Special Issue entitled Advances in High Density Lipoprotein Formation and Metabolism: A Tribute to John F. Oram (1945-2010).

Indexed as

AnimalsCoronary Artery DiseaseGenome-Wide Association StudyHumansHypercholesterolemiaHypertriglyceridemiaLipaseLipoproteinsObesityPhenotypePolymorphism, GeneticPromoter Regions, GeneticSpecific GravityLipaseLIPC protein, humanLipoproteins

Identifiers

PMID21986251
PMCPMC3288605
OpenAlexW1965730282

What OpenQuestion holds

Textmetadata
LicenceTDM
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.