Evidence map›Paper›PMID 36475519›Full record

ArticleHaematologica2023

Adipocytes control hematopoiesis and inflammation through CD40 signaling.

Myrthe E Reiche, Kikkie Poels, Laura A Bosmans, Winnie G Vos, Claudia M Van Tiel, Marion J J Gijbels, Suzanne A B M Aarts, Myrthe Den Toom, Linda Beckers, Christian Weber and 4 more

Open access · goldAbstract read
In one paragraph

Article in Haematologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Adipocytes in their (CD)40s.Haematologica · 2023
    Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 5 institutions in 5 countries.

Myrthe E ReicheDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands; Department of Medical Cell Biology, Uppsala University, Uppsala.
Kikkie PoelsDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Laura A BosmansDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Winnie G VosDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Claudia M Van TielDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Marion J J GijbelsDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands; Cardiovascular Research Institute Maastricht (CARIM), Department of Biochemistry, Maastricht University, Maastricht.
Suzanne A B M AartsDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Myrthe Den ToomDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Linda BeckersDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam.
Christian WeberCardiovascular Research Institute Maastricht (CARIM), Department of Biochemistry, Maastricht University, Maastricht, The Netherlands; Institute of Cardiovascular Prevention (IPEK), Ludwig-Maximilians Universität, Munich, Germany; German Centre of Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich.
Dorothee AtzlerInstitute of Cardiovascular Prevention (IPEK), Ludwig-Maximilians Universität, Munich, Germany; German Centre of Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich, Germany; Walther-Straub-Institute of Pharmacology and Toxicology, Ludwig-Maximilians Universität, Munich.
Patrick C N RensenDepartment of Medicine, Division of Endocrinology, and Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden.
Sander KooijmanDepartment of Medicine, Division of Endocrinology, and Einthoven Laboratory for Vascular and Regenerative Medicine, Leiden University Medical Center, Leiden.
Esther LutgensDepartment of Medical Biochemistry, Amsterdam Cardiovascular Sciences (ACS), Amsterdam University Medical Centres, University of Amsterdam, Amsterdam, The Netherlands; Institute of Cardiovascular Prevention (IPEK), Ludwig-Maximilians Universität, Munich, Germany; German Centre of Cardiovascular Research (DZHK), partner site Munich Heart Alliance, Munich, Germany; Cardiovascular Medicine, Experimental CardioVascular Immunology Laboratory, Mayo Clinic, Rochester, MN. Lutgens.Esther@mayo.edu.
Amsterdam University Medical Centers · NLUniversity of Amsterdam · NLLeiden University Medical Center · NLLudwig-Maximilians-Universität München · DEMayo Clinic in Arizona · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The co-stimulatory CD40-CD40L dyad plays an important role in chronic inflammatory diseases associated with aging. Although CD40 is mainly expressed by immune cells, CD40 is also present on adipocytes. We aimed to delineate the role of adipocyte CD40 in the aging hematopoietic system and evaluated the effects of adipocyte CD40 deficiency on cardiometabolic diseases. Adult adipocyte CD40-deficient mice (AdiCD40KO) mice had a decrease in bone marrow hematopoietic stem cells (Lin-Sca+cKit+, LSK) and common lymphoid progenitors, which was associated with increased bone marrow adiposity and T-cell activation, along with elevated plasma corticosterone levels, a phenotype that became more pronounced with age. Atherosclerotic AdiCD40koApoE-/- (CD40AKO) mice also displayed changes in the LSK population, showing increased myeloid and lymphoid multipotent progenitors, and augmented corticosterone levels. Increased T-cell activation could be observed in bone marrow, spleen, and adipose tissue, while the numbers of B cells were decreased. Although atherosclerosis was reduced in CD40AKO mice, plaques contained more activated T cells and larger necrotic cores. Analysis of peripheral adipose tissue in a diet-induced model of obesity revealed that obese AdiCD40KO mice had increased T-cell activation in adipose tissue and lymphoid organs, but decreased weight gain and improved insulin sensitivity, along with increased fat oxidation. In conclusion, adipocyte CD40 plays an important role in maintaining immune cell homeostasis in bone marrow during aging and chronic inflammatory diseases, particularly of the lymphoid populations. Although adipocyte CD40 deficiency reduces atherosclerosis burden and ameliorates diet-induced obesity, the accompanying T-cell activation may eventually aggravate cardiometabolic diseases.

Indexed as

AtherosclerosisCardiovascular DiseasesAdipocytesAnimalsCD40 AntigensCD40 LigandCorticosteroneHematopoiesisInflammationMiceMice, Inbred C57BLObesityCD40 AntigensCD40 LigandCorticosterone

Identifiers

PMID36475519
PMCPMC10316249
OpenAlexW4311720498

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.