Evidence map›Paper›PMID 35549955›Full record

ArticleCardiovascular diabetology2022

Increased frequency of proangiogenic tunica intima endothelial kinase 2 (Tie2) expressing monocytes in individuals with type 2 diabetes mellitus.

M Reijrink, J van Ark, C P H Lexis, L M Visser, M E Lodewijk, I C C van der Horst, C J Zeebregts, H van Goor, S C A de Jager, G Pasterkamp and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cardiovascular diabetology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Non-classical monocytes frequency and serum vitamin DJournal of diabetes investigation · 2023
    Article
  7. Review
  8. Article
  9. 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

12 authors at 4 institutions in 1 country.

M Reijrink *Department of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands.
J van Ark *Department of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands.
C P H LexisDepartment of Cardiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
L M VisserDepartment of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands.
M E LodewijkDepartment of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands.
I C C van der HorstDepartment of Intensive Care Medicine, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Maastricht, The Netherlands.
C J ZeebregtsDepartment of Surgery - Division of Vascular Surgery, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
H van GoorDepartment of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands.
S C A de JagerLaboratory of Experimental Cardiology, University Medical Center Utrecht, University of Utrecht, Utrecht, The Netherlands.
G PasterkampCenter Diagnostic Laboratory, Division Laboratories and Pharmacy, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
B H R WolffenbuttelDepartment of Endocrinology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
J L HillebrandsDepartment of Pathology & Medical Biology - Pathology, University of Groningen, University Medical Center Groningen, Hanzeplein 1, PO Box 30.001, Groningen, The Netherlands. j.l.hillebrands@umcg.nl.
University Medical Center Groningen · NLUniversity of Groningen · NLUtrecht University · NLMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIndividuals with type 2 diabetes mellitus (T2DM) have an increased risk for developing macrovascular disease (MVD) manifested by atherosclerosis. Phenotypically and functionally different monocyte subsets (classical; CD14

methodsIndividuals with (N = 51) and without (N = 56) T2DM were recruited and allocated to "non-MVD" or "with MVD" (i.e., peripheral or coronary artery disease) subgroups. Blood monocyte subsets were quantified based on CD14, CD16 and Tie2 expression levels. Plasma levels of Tie2-ligands angiopoietin-1 and angiopoietin-2 were determined using ELISA. Carotid endarterectomy samples from individuals with (N = 24) and without (N = 22) T2DM were stained for intraplaque CD68

resultsMonocyte counts were similar between individuals with T2DM and healthy controls (non-diabetic, non-MVD). Non-classical monocytes were reduced (p < 0.05) in T2DM, whereas the percentage of TEMs within the intermediate subset was increased (p < 0.05). T2DM was associated with increased angiopoietin-1 (p < 0.05) and angiopoietin-2 (p = 0.0001) levels. Angiopoietin-2 levels were higher in T2DM individuals with MVD compared with non-MVD (p < 0.01). Endarterectomized plaques showed no differences in macrophage influx and microvessel number between individuals with and without T2DM.

conclusionsMonocyte subset distribution is altered in T2DM with reduced non-classical monocytes and increased TEM percentage in the intermediate monocyte subset. Increased angiopoietin-2 levels together with increased frequency of TEMs might promote plaque vulnerability in T2DM which could however not be confirmed at tissue level in advanced atherosclerotic lesions.

Indexed as

AtherosclerosisDiabetes Mellitus, Type 2Plaque, AtheroscleroticAngiopoietin-1Angiopoietin-2HumansMonocytesReceptor, TIE-2Tunica IntimaAngiopoietin-1Angiopoietin-2Receptor, TIE-2TEK protein, humanAngiogenesisAtherosclerosisMacrovascular diseaseMonocyte heterogeneityMonocytesTie2Type 2 diabetes mellitus

Identifiers

PMID35549955
PMCPMC9102255
OpenAlexW4280578364

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.