Evidence map›Paper›PMID 25848123›Full record

ReviewStem cells translational medicine2015

Concise Review: Macrophages: Versatile Gatekeepers During Pancreatic β-Cell Development, Injury, and Regeneration.

Naomi Van Gassen, Willem Staels, Eva Van Overmeire, Sofie De Groef, Mozhdeh Sojoodi, Yves Heremans, Gunter Leuckx, Mark Van de Casteele, Jo A Van Ginderachter, Harry Heimberg and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Stem cells translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 41 citations in OpenAlex.

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  15. Exercise and Type 1 Diabetes.Advances in experimental medicine and biology · 2020
    Review
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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

11 authors at 4 institutions in 1 country.

Naomi Van GassenDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Willem StaelsDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Eva Van OvermeireDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Sofie De GroefDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Mozhdeh SojoodiDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Yves HeremansDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Gunter LeuckxDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Mark Van de CasteeleDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Jo A Van GinderachterDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium.
Harry HeimbergDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium Harry.Heimberg@vub.ac.be Nico.De.Leu@vub.ac.be.
Nico De LeuDiabetes Research Center and Laboratory of Cellular and Molecular Immunology, Vrije Universiteit Brussel, Brussels, Belgium; Division of Pediatric Endocrinology, Department of Pediatrics, Ghent University Hospital, and Department of Pediatrics and Genetics, Ghent University, Ghent, Belgium; Myeloid Cell Immunology Laboratory, VIB, Brussels, Belgium; Department of Endocrinology, Universitair Ziekenhuis Brussel, Brussels, Belgium Harry.Heimberg@vub.ac.be Nico.De.Leu@vub.ac.be.
Vrije Universiteit Brussel · BEVIB-VUB Laboratory Myeloid Cell Immunology · BEGhent University Hospital · BEUniversitair Ziekenhuis Brussel · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledMacrophages are classically considered detrimental for pancreatic β-cell survival and function, thereby contributing to β-cell failure in both type 1 (T1D) and 2 (T2D) diabetes mellitus. In addition, adipose tissue macrophages negatively influence peripheral insulin signaling and promote obesity-induced insulin resistance in T2D. In contrast, recent data unexpectedly uncovered that macrophages are not only able to protect β cells during pancreatitis but also to orchestrate β-cell proliferation and regeneration after β-cell injury. Moreover, by altering their activation state, macrophages are able to improve insulin resistance in murine models of T2D. This review will elaborate on current insights in macrophage heterogeneity and on the evolving role of pancreas macrophages during organogenesis, tissue injury, and repair. Additional identification of macrophage subtypes and of their secreted factors might ultimately translate into novel therapeutic strategies for both T1D and T2D. SIGNIFICANCE: Diabetes mellitus is a pandemic disease, characterized by severe acute and chronic complications. Macrophages have long been considered prime suspects in the pathogenesis of both type 1 and 2 diabetes mellitus. In this concise review, current insights in macrophage heterogeneity and on the, as yet, underappreciated role of alternatively activated macrophages in insulin sensing and β-cell development/repair are reported. Further identification of macrophage subtypes and of their secreted factors might ultimately translate into novel therapeutic strategies for diabetes mellitus.

Indexed as

RegenerationAnimalsDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2HumansInsulin-Secreting CellsMacrophagesPancreatitisDevelopmentInjuryMacrophagePancreasRegenerationβ Cell

Identifiers

PMID25848123
PMCPMC4449100
OpenAlexW2041008010

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.