Evidence map›Paper›PMID 41261284›Full record

ArticleEMBO reports2025

Purinergic adipocyte-macrophage crosstalk promotes degeneration of thermogenic brown adipose tissue.

Michelle Y Jaeckstein, Alexander W Fischer, Björn Rissiek, Tobias Staehler, Markus Heine, Janina Behrens, Oliver Mann, Alexander Pfeifer, Tim Magnus, Christian Schlein and 4 more

Abstract read
In one paragraph

Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

14 authors.

Michelle Y JaecksteinDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Alexander W FischerDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Björn RissiekDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0001-5327-5479
Tobias StaehlerInstitute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0002-0845-3800
Markus HeineDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Janina BehrensDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Oliver MannDepartment of General, Visceral and Thoracic Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Alexander PfeiferInstitute of Pharmacology and Toxicology, University Hospital, University of Bonn, Bonn, Germany.ORCID 0000-0001-8805-6831
Tim MagnusDepartment of Neurology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Christian SchleinInstitute of Human Genetics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anna WorthmannDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Ludger SchejaDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Friedrich Koch-NolteInstitute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID 0000-0003-1730-6674
Joerg HeerenDepartment of Biochemistry and Molecular Cell Biology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. heeren@uke.de.ORCID 0000-0002-5647-1034

Funding

Deutsche Forschungsgemeinschaft (DFG) 335447727Deutsche Forschungsgemeinschaft (DFG) 450149205
6 · The paper itself

Abstract

Loss of brown adipose tissue (BAT) activity observed during ageing, obesity and living at thermoneutrality is associated with lipid accumulation, fibrosis and tissue inflammation in BAT. The mechanisms that promote this degenerative process of BAT remain largely enigmatic. Here, we show that an imbalance between sympathetic activation and mitochondrial energy handling causes BAT degeneration, which leads to impaired energy expenditure and systemic metabolic disturbances. Mechanistically, we demonstrate that brown adipocytes secrete ATP in response to imbalanced thermogenic activation, which activates P2X4 and P2X7 of BAT-resident macrophages. Notably, mice lacking activity of these purinergic receptors in myeloid cells are protected against BAT inflammation, thermogenic dysfunction and systemic metabolic disturbances under conditions of imbalanced BAT activation, thermoneutrality or overnutrition. These results highlight the relevance of extracellular ATP released by brown adipocytes as a paracrine signal for myeloid cells to initiate BAT degeneration.

Indexed as

Adipocytes, BrownAdipose Tissue, BrownMacrophagesThermogenesisAdenosine TriphosphateAnimalsEnergy MetabolismInflammationMiceMice, Inbred C57BLReceptors, Purinergic P2X4Receptors, Purinergic P2X7Adenosine TriphosphateReceptors, Purinergic P2X4Receptors, Purinergic P2X7Adaptive ThermogenesisDyslipidemiaHyperglycemiaInflammationP2X Receptors

Identifiers

PMID41261284
PMCPMC12715258

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.