Evidence map›Paper›PMID 17200713›Full record

ArticleThe Journal of clinical investigation2007

Atherogenic remnant lipoproteins: role for proteoglycans in trapping, transferring, and internalizing.

Robert W Mahley, Yadong Huang

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
4.7field-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

82 citing papers in PubMed, 155 citations in OpenAlex.

  1. Trial
  2. Article
  3. Current and Emerging Pharmacological Therapies for Hypertriglyceridemia.International journal of molecular sciences · 2026
    Review
  4. Article
  5. Rodent Models for Atherosclerosis.International journal of molecular sciences · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Metabolism of Triglyceride-Rich Lipoproteins.Handbook of experimental pharmacology · 2022
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Robert W MahleyGladstone Institute of Neurological Disease and Gladstone Institute of Cardiovascular Disease, San Francisco, California 94158, USA. rmahley@gladstone.ucsf.edu
Yadong Huang
Gladstone Institutes · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unraveling the mechanisms controlling remnant lipoprotein clearance is important, as these lipoproteins are highly atherogenic. The most critical molecule in this process is apoE, which mediates high-affinity binding of remnant lipoproteins to members of the LDL receptor (LDLR) family and cell-surface heparan sulfate proteoglycans (HSPGs), which have been shown to play major independent as well as cooperative roles in remnant lipoprotein clearance. While all the players may have been identified, our understanding of how they interact and function together continues to evolve. In this issue of the JCI, MacArthur et al. (see the related article beginning on page 153) demonstrated that HSPGs under normal physiological conditions are critically important in the clearance of remnant lipoproteins, independent of LDLR family members. The complexity of VLDL and chylomicron remnant clearance was exemplified by the studies of Jones et al., also in this issue (see the related article beginning on page 165). Despite defective clearance of LDL in mice with a deficiency in the adaptor protein controlling internalization of the LDLR, called autosomal recessive hypercholesterolemia (ARH), remnant lipoprotein clearance was not grossly abnormal. A likely explanation is that the abnormal LDLRs bind the remnants and then transfer them to another acceptor for internalization. While the studies clearly demonstrate that the LDLR-related protein 1 is not involved and suggest a role for an additional unidentified receptor, it remains a possibility that HSPGs are responsible for remnant uptake by hepatocytes in the presence of defective LDLR internalization.

Indexed as

AtherosclerosisBiological TransportHeparan Sulfate ProteoglycansHumansLipoproteinsLiverModels, BiologicalProteoglycansReceptors, LDLTriglyceridesHeparan Sulfate ProteoglycansLipoproteinsProteoglycansReceptors, LDLTriglycerides

Identifiers

PMID17200713
PMCPMC1716223
OpenAlexW2047465218

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.