Evidence map›Paper›PMID 41484108›Full record

ArticleNature communications2026

Non-remnant triglyceride-rich lipoproteins due to lipoprotein lipase deficiency increase atherosclerosis in mice.

Ainara G Cabodevilla, Maria Concepcion Izquierdo, Debapriya Basu, Waqas Younis, Munichandra Babu Tirumalasetty, Qing Robert Miao, Dimitris Nasias, Jenny E Kanter, Tse Wing Winnie Ho, Jana Gjini and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Ainara G Cabodevilla *Division of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Maria Concepcion Izquierdo *Division of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Debapriya BasuDivision of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Waqas YounisDivision of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Munichandra Babu TirumalasettyDepartment of the Foundations of Medicine, NYU-Long Island School of Medicine, Mineola, NY, USA.ORCID http://orcid.org/0000-0002-0177-7925
Qing Robert MiaoDepartment of the Foundations of Medicine, NYU-Long Island School of Medicine, Mineola, NY, USA.ORCID http://orcid.org/0000-0002-3125-1238
Dimitris NasiasDivision of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Jenny E KanterDivision of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA, USA.ORCID http://orcid.org/0000-0003-3212-772X
Tse Wing Winnie HoKeenan Centre for Biomedical Research, St. Michael's Hospital and Division of Critical Care, Department of Medicine, University of Toronto, Toronto, ON, Canada.ORCID http://orcid.org/0000-0003-4465-7859
Jana GjiniDivision of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA.
Edward FisherDivision of Cardiology, Department of Medicine, New York University Grossman School of Medicine, New York, NY, USA.ORCID http://orcid.org/0000-0001-9802-143X
Jeffrey KimComparative Medicine Research Unit, University of Louisville School of Medicine, Louisville, KY, USA.
Warren L LeeKeenan Centre for Biomedical Research, St. Michael's Hospital and Division of Critical Care, Department of Medicine, University of Toronto, Toronto, ON, Canada.ORCID http://orcid.org/0000-0002-1788-6587
Karin BornfeldtDivision of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington, Seattle, WA, USA.ORCID http://orcid.org/0000-0001-9208-6523
Ira J GoldbergDivision of Endocrinology, Diabetes and Metabolism, New York University Grossman School of Medicine, New York, NY, USA. Ira.Goldberg@nyulangone.org.ORCID http://orcid.org/0000-0002-8701-2201

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Triglycerides, Diabetes and Cardiovascular DiseaseP01HL151328 · NHLBI · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 2020 to 2026
$19.6M
Novel regulatory mechanisms controlling hepatic apoB-Lp lipid loading and secretionP01HL160470 · NHLBI · NYU LONG ISLAND SCHOOL OF MEDICINE · PI M Mahmood Hussain · 2023 to 2026
$12.3M
Identifying new strategies for prevention of cardiovascular complications of diabetesR35HL150754 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E · 2020 to 2025
$6.2M
Cholesterol reduction and cardiovascular risk in Type 1 diabetesR01HL164949 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Ira J Goldberg · 2022 to 2026
$4.0M
NHLBI NIH HHS P01 HL151328NHLBI NIH HHS P01 HL160470NHLBI NIH HHS R01 HL164949NHLBI NIH HHS R35 HL150754NIDDK NIH HHS P30 DK017047U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL160470U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL164949U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) P01HL151328U.S. Department of Health & Human Services | NIH | National Heart, Lung, and Blood Institute (NHLBI) R35HL150754
6 · The paper itself

Abstract

Increased fasting and postprandial triglyceride levels are risk factors for cardiovascular disease (CVD). Partially metabolized triglyceride-rich lipoproteins (TRLs) termed remnants are created when intestinally-derived chylomicrons and liver secreted very low density lipoproteins (VLDLs) interact with lipoprotein lipase (LpL) situated on the luminal surface of capillary endothelial cells. Higher circulating remnant levels have been implicated as the reason for the relationship between TRL levels and CVD. We hypothesized that nascent lipoproteins not only remnants are atherogenic. To test this, we created mice with induced whole-body lipoprotein lipase (LpL) deficiency combined with LDL receptor (LDLR) deficiency. On an atherogenic Western-type diet (WD), male and female mice with induced global LpL deficiency (iLpl

Indexed as

AtherosclerosisLipoprotein LipaseLipoproteinsTriglyceridesAnimalsAortaCholesterolChylomicronsDiet, WesternEndothelial CellsFemaleHypertriglyceridemiaLipoproteins, VLDLMaleMiceMice, Inbred C57BLCholesterolChylomicronsLipoprotein LipaseLipoproteinsLipoproteins, VLDLlipoprotein triglycerideReceptors, LDLTriglycerides

Identifiers

PMID41484108
PMCPMC12887055

What OpenQuestion holds

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Registered trials

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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.