Evidence map›Paper›PMID 20056946›Full record

ReviewCirculation research2010

The impact of macrophage insulin resistance on advanced atherosclerotic plaque progression.

Ira Tabas, Alan Tall, Domenico Accili

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Observational
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

6 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

3 authors at 1 institution in 1 country.

Ira TabasDepartment of Medicine, Columbia University, 630 West 168th St, New York, NY 10032, USA. iat1@columbia.edu
Alan Tall
Domenico Accili
Tisch Hospital · US

Funding

TTC39B in obesity and atherosclerosisP01HL087123 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TALL, ALAN RICHARD · 2007 to 2022
$31.2M
Regulation and function of plasma lipid transfer proteinsP01HL054591 · NHLBI · ROCKEFELLER UNIVERSITY · PI GOLDBERG, IRA J · 1995 to 2010
$19.9M
The Unfolded Protein Response in Sterol CytoxicityR01HL075662 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TABAS, IRA A · 2004 to 2017
$5.6M
NHLBI NIH HHS HL054591NHLBI NIH HHS HL075662NHLBI NIH HHS HL087123NHLBI NIH HHS P01 HL054591NHLBI NIH HHS P01 HL087123NHLBI NIH HHS R01 HL075662
6 · The paper itself

Abstract

Atherothrombotic vascular disease is the major cause of death and disability in obese and diabetic subjects with insulin resistance. Although increased systemic risk factors in the setting of insulin resistance contribute to this problem, it is likely exacerbated by direct effects of insulin resistance on the arterial wall cells that participate in atherosclerosis. A critical process in the progression of subclinical atherosclerotic lesions to clinically relevant lesions is necrotic breakdown of plaques. Plaque necrosis, which is particularly prominent in the lesions of diabetics, is caused by the combination of macrophage apoptosis and defective phagocytic clearance, or efferocytosis, of the apoptotic macrophages. One cause of macrophage apoptosis in advanced plaques is activation of a proapoptotic branch of the unfolded protein response, which is an endoplasmic reticulum stress pathway. Macrophages have a functional insulin receptor signaling pathway, and downregulation of this pathway in the setting insulin resistance enhances unfolded protein response-induced apoptosis. Moreover, other aspects of the obesity/insulin-resistance syndrome may adversely affect efferocytosis. These processes may therefore provide an important mechanistic link among insulin resistance, plaque necrosis, and atherothrombotic vascular disease and suggest novel therapeutic approaches to this expanding health problem.

Indexed as

ApoptosisInsulin ResistanceSignal TransductionUnfolded Protein ResponseAnimalsArteriesAtherosclerosisEndoplasmic ReticulumHumansMacrophagesNecrosisObesityReceptor, InsulinSyndromeThrombosisReceptor, Insulin

Identifiers

PMID20056946
PMCPMC2805467
OpenAlexW2113485831

What OpenQuestion holds

Textmetadata
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.