Evidence map›Paper›PMID 28752048›Full record

ArticleMolecular metabolism2017

Myeloid protein tyrosine phosphatase 1B (PTP1B) deficiency protects against atherosclerotic plaque formation in the ApoE

D Thompson, N Morrice, L Grant, S Le Sommer, K Ziegler, P Whitfield, N Mody, H M Wilson, M Delibegović

Open access · goldAbstract read
In one paragraph

Article in Molecular metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. PTP1B inhibition promotes microglial phagocytosis in Alzheimer's disease models by enhancing SYK signaling.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  17. Eicosanoids: Atherosclerosis and cardiometabolic health.Journal of clinical & translational endocrinology · 2020
    Review
  18. Review
  19. The Antitumor Efficacy ofBioMed research international · 2020
    Review
  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

9 authors at 2 institutions in 1 country.

D ThompsonInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK. Electronic address: dthompson@abdn.ac.uk.
N MorriceInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
L GrantInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
S Le SommerInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
K ZieglerDepartment of Diabetes and Cardiovascular Science, University of the Highlands and Islands, Centre for Health Science, Inverness, UK.
P WhitfieldDepartment of Diabetes and Cardiovascular Science, University of the Highlands and Islands, Centre for Health Science, Inverness, UK.
N ModyInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
H M WilsonInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK.
M DelibegovićInstitute of Medicine, Medical Sciences and Nutrition, University of Aberdeen, Aberdeen, UK. Electronic address: m.delibegovic@abdn.ac.uk.
University of Aberdeen · GBUniversity of the Highlands and Islands · GB

Funding

British Heart Foundation PG/11/8/28703British Heart Foundation PG/14/43/30889
6 · The paper itself

Abstract

objectiveCardiovascular disease (CVD) is the most prevalent cause of mortality among patients with Type 1 or Type 2 diabetes, due to accelerated atherosclerosis. Recent evidence suggests a strong link between atherosclerosis and insulin resistance due to impaired insulin receptor (IR) signaling. Moreover, inflammatory cells, in particular macrophages, play a key role in pathogenesis of atherosclerosis and insulin resistance in humans. We hypothesized that inhibiting the activity of protein tyrosine phosphatase 1B (PTP1B), the major negative regulator of the IR, specifically in macrophages, would have beneficial anti-inflammatory effects and lead to protection against atherosclerosis and CVD.

methodsWe generated novel macrophage-specific PTP1B knockout mice on atherogenic background (ApoE

resultsMyeloid-PTP1B knockout mice on atherogenic background (ApoE

conclusionsHere we demonstrate that inhibiting the activity of PTP1B specifically in myeloid lineage cells protects against atherosclerotic plaque formation, under atherogenic conditions, in an ApoE

Indexed as

AMP-Activated Protein Kinase KinasesAnimalsApolipoproteins EAtherosclerosisCells, CulturedDinoprostoneFemaleInterleukin-10MacrophagesMaleMicePlaque, AtheroscleroticProtein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1AMP-Activated Protein Kinase KinasesApolipoproteins EDinoprostoneInterleukin-10Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, mouseAMPKAtherosclerosisInsulin resistanceInterleukin-10PTP1B

Identifiers

PMID28752048
PMCPMC5518727
OpenAlexW2626021295

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.