Evidence map›Paper›PMID 26892959›Full record

ReviewCirculation research2016

Surprises From Genetic Analyses of Lipid Risk Factors for Atherosclerosis.

Kiran Musunuru, Sekar Kathiresan

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
15.5field-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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 155 citations in OpenAlex.

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  10. Exploring Neutrophil Extracellular Traps in Cardiovascular Pathologies: The Impact of Lipid Profiles, PAD4, and Radiation.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2025
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25 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

2 authors at 2 institutions in 1 country.

Kiran MusunuruFrom the Department of Medicine, Harvard Medical School, Boston, MA (K.M., S.K.); Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA (K.M.); Broad Institute of MIT and Harvard, Cambridge, MA (K.M., S.K.); and Center for Human Genetic Research and Cardiovascular Research Center, Massachusetts General Hospital, Boston (S.K.).
Sekar KathiresanFrom the Department of Medicine, Harvard Medical School, Boston, MA (K.M., S.K.); Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA (K.M.); Broad Institute of MIT and Harvard, Cambridge, MA (K.M., S.K.); and Center for Human Genetic Research and Cardiovascular Research Center, Massachusetts General Hospital, Boston (S.K.). skathiresan@partners.org.
Center for Human Genetics · USHarvard University · US

Funding

Research Training in Pulmonary Immunology and Allergy at MGHT32HL116275 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI David C Christiani, ANDREW D LUSTER · 2013 to 2026
$8.6M
Discovery of Mendelian Dyslipidemia and Heart Attack Genes Using Exome SequencingR01HL107816 · NHLBI · MASSACHUSETTS GENERAL HOSPITAL · PI KATHIRESAN, SEKAR · 2011 to 2015
$2.7M
NHLBI NIH HHS R01 HL107816NHLBI NIH HHS T32 HL116275
6 · The paper itself

Abstract

Observational epidemiological studies have associated plasma lipid concentrations with risk for coronary heart disease (CHD), but these studies cannot distinguish cause from mere correlation. Human genetic studies, when considered with the results of randomized controlled trials of medications, can potentially shed light on whether lipid biomarkers are causal for diseases. Genetic analyses and randomized trials suggest that low-density lipoprotein is causal for CHD, whereas high-density lipoprotein is not. Surprisingly, human genetic evidence suggests that lipoprotein(a) and triglyceride-rich lipoproteins causally contribute to CHD. Gene variants leading to higher levels of plasma apolipoprotein B-containing lipoproteins [low-density lipoprotein, triglyceride-rich lipoproteins, or lipoprotein(a)] consistently increase risk for CHD. For triglyceride-rich lipoproteins, the most compelling evidence revolves around lipoprotein lipase and its endogenous facilitator (APOA5 [apolipoprotein A-V]) and inhibitory proteins (APOC3 [apolipoprotein C-III], ANGPTL4 [angiopoietin like 4]). Combined, these genetic results anticipate that, beyond low-density lipoprotein, pharmacological lowering of triglyceride-rich lipoproteins or lipoprotein(a) will reduce risk for CHD, but this remains to be proven through randomized controlled trials.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAnimalsCholesterol, HDLCholesterol, LDLCoronary Artery DiseaseDyslipidemiasGenetic MarkersGenetic Predisposition to DiseaseHumansHypolipidemic AgentsLipid MetabolismLipoprotein(a)PhenotypePrimary PreventionPrognosisRisk Assessment1-Alkyl-2-acetylglycerophosphocholine EsteraseCholesterol, HDLCholesterol, LDLGenetic MarkersHypolipidemic AgentsLipoprotein(a)PLA2G7 protein, humanTriglyceridesatherosclerosiscoronary diseasegeneticslipoproteinstriglycerides

Identifiers

PMID26892959
PMCPMC4762058
OpenAlexW2286634515

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.