Evidence map›Paper›PMID 29419410›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2018

2017 George Lyman Duff Memorial Lecture: Fat in the Blood, Fat in the Artery, Fat in the Heart: Triglyceride in Physiology and Disease.

Ira J Goldberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
4.6field-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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  16. Renin-Angiotensin System and Cardiovascular Functions.Arteriosclerosis, thrombosis, and vascular biology · 2018
    Review
  17. 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

1 author at 1 institution in 2 countries.

Ira J GoldbergFrom the Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, New York University School of Medicine. Ira.Goldberg@NYUMC.org.
Diabetes Australia · AU

Funding

Pathways of Tissue Lipid UptakeR01HL045095 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ABUMRAD, NADA A., GOLDBERG, IRA J · 1991 to 2024
$6.9M
Mechanisms of Fatty Acid Uptake By Cardiac MuscleR01HL073029 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI GOLDBERG, IRA J · 2003 to 2021
$6.8M
Diabetes-Mediated Effects on Myeloid Precursors and Vascular ComplicationsR01DK095684 · NIDDK · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A, GOLDBERG, IRA J · 2012 to 2016
$2.7M
NHLBI NIH HHS R01 HL045095NHLBI NIH HHS R01 HL073029NIDDK NIH HHS R01 DK095684
6 · The paper itself

Abstract

Cholesterol is not the only lipid that causes heart disease. Triglyceride supplies the heart and skeletal muscles with highly efficient fuel and allows for the storage of excess calories in adipose tissue. Failure to transport, acquire, and use triglyceride leads to energy deficiency and even death. However, overabundance of triglyceride can damage and impair tissues. Circulating lipoprotein-associated triglycerides are lipolyzed by lipoprotein lipase (LpL) and hepatic triglyceride lipase. We inhibited these enzymes and showed that LpL inhibition reduces high-density lipoprotein cholesterol by >50%, and hepatic triglyceride lipase inhibition shifts low-density lipoprotein to larger, more buoyant particles. Genetic variations that reduce LpL activity correlate with increased cardiovascular risk. In contrast, macrophage LpL deficiency reduces macrophage function and atherosclerosis. Therefore, muscle and macrophage LpL have opposite effects on atherosclerosis. With models of atherosclerosis regression that we used to study diabetes mellitus, we are now examining whether triglyceride-rich lipoproteins or their hydrolysis by LpL affect the biology of established plaques. Following our focus on triglyceride metabolism led us to show that heart-specific LpL hydrolysis of triglyceride allows optimal supply of fatty acids to the heart. In contrast, cardiomyocyte LpL overexpression and excess lipid uptake cause lipotoxic heart failure. We are now studying whether interrupting pathways for lipid uptake might prevent or treat some forms of heart failure.

Indexed as

Plaque, AtheroscleroticAnimalsArteriesAtherosclerosisHeartHeart FailureHumansHydrolysisHypertriglyceridemiaHypolipidemic AgentsLipoprotein LipaseLipoproteinsMyocardiumRisk FactorsTriglyceridesHypolipidemic AgentsLipoprotein LipaseLipoproteinsLPL protein, humanTriglyceridesatherosclerosisfatty acidsheart failurelipoprotein lipasetriglycerides

Identifiers

PMID29419410
PMCPMC5864527
OpenAlexW2914661299

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.