Evidence map›Paper›PMID 24751561›Full record

ReviewAnnals of global health

Regression of atherosclerosis: insights from animal and clinical studies.

Jonathan E Feig

Abstract readReview
In one paragraph

Review in Annals of global health. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Survey of Approaches for Investigation of Atherosclerosis In Vivo.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  9. Article
  10. Article
  11. Role of vitamin D in the pathogenesis of atheromatosis.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Vulnerable Plaque, Characteristics, Detection, and Potential Therapies.Journal of cardiovascular development and disease · 2019
    Review
  18. Review
  19. Article
  20. 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

1 author.

Jonathan E FeigZena and Michael A. Wiener Cardiovascular Institute, Mount Sinai Medical Center, New York, NY. Electronic address: jonathan.feig@mountsinai.org.

Funding

Regression of Atherosclerosis CoreP01HL098055 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI HAZEN, STANLEY L · 2010 to 2014
$12.1M
Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
Role and Regulation of CCR7 in Regression of Atherosclerotic LesionsF30AG029748 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FEIG, JONATHAN E · 2007 to 2010
$170k
NHLBI NIH HHS HL-084312NHLBI NIH HHS HL-098055NHLBI NIH HHS R01 HL084312NIA NIH HHS AG-029748NIA NIH HHS F30 AG029748
6 · The paper itself

Abstract

backgroundBased on studies that date back to the 1920s, regression and stabilization of atherosclerosis in humans has gone from just a dream to one that is achievable. Review of the literature indicates that the successful attempts at regression generally applied robust measures to improve plasma lipoprotein profiles. Examples include extensive lowering of plasma concentrations of atherogenic apolipoprotein B and enhancement of reverse cholesterol transport from atheromata to the liver.

findingsPossible mechanisms responsible for lesion shrinkage include decreased retention of atherogenic apolipoprotein B within the arterial wall, efflux of cholesterol and other toxic lipids from plaques, emigration of lesional foam cells out of the arterial wall, and influx of healthy phagocytes that remove necrotic debris as well as other components of the plaque. This review will highlight the role key players such as LXR, HDL and CCR7 have in mediating regression.

conclusionAlthough much progress has been made, there are many unanswered questions. There is, therefore, a clear need for preclinical and clinical testing of new agents expected to facilitate atherosclerosis regression with the hope that additional mechanistic insights will allow further progress.

Indexed as

AnimalsApolipoproteins BAtherosclerosisCholesterol Ester Transfer ProteinsCholesterol, HDLCholesterol, LDLCoronary VesselsFoam CellsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLiver X ReceptorsMagnetic Resonance ImagingNiacinOrphan Nuclear ReceptorsReceptors, CCR7Tomography, Optical CoherenceApolipoproteins BCCR7 protein, humanCholesterol Ester Transfer ProteinsCholesterol, HDLCholesterol, LDLHydroxymethylglutaryl-CoA Reductase InhibitorsLiver X ReceptorsNiacinOrphan Nuclear ReceptorsReceptors, CCR7atherosclerosisCCR7HDLmacrophagesregression

Identifiers

PMID24751561
PMCPMC4262135

What OpenQuestion holds

Texttitle and abstract
LicenceTDM
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.