Evidence map›Paper›PMID 21670500›Full record

ArticleThe Journal of clinical investigation2011

The VLDL receptor promotes lipotoxicity and increases mortality in mice following an acute myocardial infarction.

Jeanna C Perman, Pontus Boström, Malin Lindbom, Ulf Lidberg, Marcus StÅhlman, Daniel Hägg, Henrik Lindskog, Margareta Scharin Täng, Elmir Omerovic, Lillemor Mattsson Hultén and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 2% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  6. Review
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  14. Article
  15. SIRT1 regulates hepatic vldlr levels.Cell communication and signaling : CCS · 2024
    Article
  16. Review
  17. Cardiac Metabolism, Reprogramming, and Diseases.Journal of cardiovascular translational research · 2024
    Review
  18. Article
  19. Review
  20. Article

24 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

18 authors at 3 institutions in 2 countries.

Jeanna C PermanSahlgrenska Center for Cardiovascular and Metabolic Research, Wallenberg Laboratory, Sahlgrenska University Hospital, Göteborg, Sweden.
Pontus Boström
Malin Lindbom
Ulf Lidberg
Marcus StÅhlman
Daniel Hägg
Henrik Lindskog
Margareta Scharin Täng
Elmir Omerovic
Lillemor Mattsson Hultén
Anders Jeppsson
Petur Petursson
Johan Herlitz
Gunilla Olivecrona
Dudley K Strickland
Kim Ekroos
Sven-Olof Olofsson
Jan Borén
Sahlgrenska University Hospital · SEUmeå University · SEZora Biosciences (Finland) · FI

Funding

tPA and LRP in StrokeP01HL054710 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STRICKLAND, DUDLEY K. · 1996 to 2011
$17.3M
NHLBI NIH HHS HL054710NHLBI NIH HHS P01 HL054710
6 · The paper itself

Abstract

Impaired cardiac function is associated with myocardial triglyceride accumulation, but it is not clear how the lipids accumulate or whether this accumulation is detrimental. Here we show that hypoxia/ischemia-induced accumulation of lipids in HL-1 cardiomyocytes and mouse hearts is dependent on expression of the VLDL receptor (VLDLR). Hypoxia-induced VLDLR expression in HL-1 cells was dependent on HIF-1α through its interaction with a hypoxia-responsive element in the Vldlr promoter, and VLDLR promoted the endocytosis of lipoproteins. Furthermore, VLDLR expression was higher in ischemic compared with nonischemic left ventricles from human hearts and was correlated with the total lipid droplet area in the cardiomyocytes. Importantly, Vldlr-/- mice showed improved survival and decreased infarct area following an induced myocardial infarction. ER stress, which leads to apoptosis, is known to be involved in ischemic heart disease. We found that ischemia-induced ER stress and apoptosis in mouse hearts were reduced in Vldlr-/- mice and in mice treated with antibodies specific for VLDLR. These findings suggest that VLDLR-induced lipid accumulation in the ischemic heart worsens survival by increasing ER stress and apoptosis.

Indexed as

AnimalsApoptosisCell LineEndoplasmic ReticulumHumansLipid MetabolismLipidsMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardial IschemiaMyocardiumReceptors, LDLStress, PhysiologicalSurvival RateLipidsReceptors, LDLTriglyceridesVLDL receptor

Identifiers

PMID21670500
PMCPMC3223818
OpenAlexW2078845557

What OpenQuestion holds

Textmetadata
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.