Evidence map›Paper›PMID 26642235›Full record

ReviewJournal of biomedical research2016

HDL signaling and protection against coronary artery atherosclerosis in mice.

Bernardo L Trigatti, Mark Fuller

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of biomedical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Proteomic Exploration of Paraoxonase 1 Function in Health and Disease.International journal of molecular sciences · 2023
    Review
  5. HBV Infection-RelatedJournal of immunology research · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Do the Apoe-/- and Ldlr-/- Mice Yield the Same Insight on Atherogenesis?Arteriosclerosis, thrombosis, and vascular biology · 2016
    Review
  12. Article
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

2 authors at 1 institution in 1 country.

Bernardo L TrigattiDepartment of Biochemistry and Biomedical Sciences, McMaster University and Thrombosis and Atherosclerosis Research Institute, McMaster University and Hamilton Health Sciences., Hamilton, Ontario L8L 2X2, Canada; trigatt@mcmaster.ca.
Mark FullerDepartment of Biochemistry and Biomedical Sciences, McMaster University and Thrombosis and Atherosclerosis Research Institute, McMaster University and Hamilton Health Sciences., Hamilton, Ontario L8L 2X2, Canada.
Thrombosis and Atherosclerosis Research Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a leading underlying factor in cardiovascular disease and stroke, important causes of morbidity and mortality across the globe. Abundant epidemiological studies demonstrate that high levels of high density lipoprotein (HDL) are associated with reduced risk of atherosclerosis and preclinical, animal model studies demonstrate that this association is causative. Understanding the molecular mechanisms underlying the protective effects of HDL will allow more strategic approaches to development of HDL based therapeutics. Recent evidence suggests that an important aspect of the ability of HDL to protect against atherosclerosis is its ability to trigger signaling responses in a variety of target cells including endothelial cells and macrophages in the vessel wall. These signaling responses require the HDL receptor, scavenger receptor class B type 1 (SR-B1), an adaptor protein (PDZK1) that binds to the cytosolic C terminus of SR-B1, Akt1 activation and (at least in endothelial cells) activation of endothelial NO synthase (eNOS). Mouse models of atherosclerosis, exemplified by apolipoprotein E or low density lipoprotein receptor gene inactivated mice (apoE or LDLR KO) develop atherosclerosis in their aortas but appear generally resistant to coronary artery atherosclerosis. On the other hand, inactivation of each of the components of HDL signaling (above) in either apoE or LDLR KO mice renders them susceptible to extensive coronary artery atherosclerosis suggesting that HDL signaling may play an important role in protection against coronary artery disease.

Indexed as

coronary artery diseasehigh density lipoproteinmyocardial infarctionscavenger receptor class B type 1

Identifiers

PMID26642235
PMCPMC4820886
OpenAlexW2466404979

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.