Evidence map›Paper›PMID 28428482›Full record

ReviewJournal of atherosclerosis and thrombosis2017

Triglyceride Rich Lipoprotein -LPL-VLDL Receptor and Lp(a)-VLDL Receptor Pathways for Macrophage Foam Cell Formation.

Sadao Takahashi

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-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

26 citing papers in PubMed, 64 citations in OpenAlex.

  1. Review
  2. Hypertriglyceridemia: Molecular and Genetic Landscapes.International journal of molecular sciences · 2024
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Role of macrophage scavenger receptor 1 in the progression of dyslipidemia in acne vulgaris patients.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2023
    Article
  8. Article
  9. Article
  10. New insight into dyslipidemia-induced cellular senescence in atherosclerosis.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  11. Review
  12. Observational
  13. Review
  14. Review
  15. Review
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  17. Review
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  19. Article
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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

1 author at 1 institution in 1 country.

Sadao TakahashiDivision of Diabetes, Ageo Central General Hospital.
Hakodate Central General Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Very low-density lipoprotein (VLDL) receptor is a member of the low-density lipoprotein (LDL) receptor family. It binds triglyceride rich lipoprotein (TGRL) but not LDL, because it recognizes apolipoprotein (apo)E only but not apoB. The VLDL receptor functions as a peripheral lipoprotein receptor in concert with lipoprotein lipase (LPL) in heart, muscle, adipose tissue and macrophages. In contrast to the LDL receptor, VLDL receptor binds apo E2/2 VLDL and apoE3/3 VLDL particles, and its expression is not down-regulated by intracellular lipoproteins. It has been reported that both LDL-cholesterol (LDL-C) and postprandial triglyceride (chyromicron and VLDL remnants) are risk factors for human atherosclerotic cardiovascular disease (ASCVD). True ligands such as lipoprotein particles of the VLDL receptor are chyromicron remnant (CMR) and VLDL remnant (postprandial hyperlipidemia). Although the oxidized LDL (oxLDL)-scavenger receptors pathway is considered to be the main mechanism for macrophage foam cell formation, it seems that the TGRL-LPL-VLDL receptor pathway is also involved. Since Lp(a) is one of the ligands for the VLDL receptor, the Lp(a)-VLDL receptor pathway is another potential alternative. The expression of VLDL receptor protein in mouse macrophages is modest compared to that in rabbit and human macrophages, both in vitro and in vivo. Therefore, we need to elucidate the mechanism of human ASCVD not by using the mouse model and scavenger receptors pathway but instead using the rabbit model and VLDL receptor pathway, respectively.

Indexed as

Adipose TissueAnimalsApolipoprotein B-48AtherosclerosisCardiovascular DiseasesFoam CellsHumansLigandsLipoprotein LipaseLipoproteins, VLDLMacrophagesMiceMice, KnockoutMuscle, SkeletalMyocardiumRabbitsApolipoprotein B-48LigandsLipoprotein LipaseLipoproteins, VLDLReceptors, LDLReceptors, ScavengerTriglyceridesvery low density lipoprotein triglycerideVLDL receptorAtherosclerosisLipoprotein lipaseLp(a)Macrophage foam cell formationVLDL receptor

Identifiers

PMID28428482
PMCPMC5453679
OpenAlexW2606386991

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.