Evidence mapPaperPMID 41717842Full record

ReviewJournal of biochemistry2026

Innate immune signalling in the adipocyte.

Phillip A Dumesic

Abstract readReview
In one paragraph

Review in Journal of biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

1 author.

Phillip A DumesicDiabetes Center, University of California, 513 Parnassus Ave, San Francisco, CA 94143, USA.ORCID 0000-0002-5843-2864

Funding

UCSF Type 1 Diabetes Research CenterP30DK135103 · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2025 to 2025
$1.8M
Translational regulation of PGC1alpha and oxidative metabolismR00DK125722 · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · 2025 to 2025
$249k
Larry L. Hillblom Foundation Start-Up Grant 2025-D-066-SUPNIDDK NIH HHS P30 DK135103NIDDK NIH HHS R00 DK125722NIH HHS R00 DK125722 and P30 DK135103
6 · The paper itself

Abstract

Innate immune receptors detect molecular features of pathogen presence and cellular damage, enabling cells to mount anti-microbial defences including the secretion of proinflammatory cytokines. Though classically studied in immunocytes, a remarkably broad range of innate immune receptor activity is now recognized in adipocytes, including that of Toll-like receptors, NOD-like receptors, inflammasomes and nucleic acid sensors such as cGAS-STING and RIG-I. These receptors influence adipocyte proinflammatory potential through control of secreted signalling factors that act in adipose tissue. Through less well-understood mechanisms, they also influence adipocyte insulin sensitivity, lipolysis, fatty acid oxidation and thermogenesis. Innate immune receptors are activated by a diverse array of stimuli, including circulating signalling factors and intracellular metabolic stresses, especially those related to mitochondrial function. The receptors are thus a potential means by which obesity-associated signals act through adipocytes to drive inflammation, adipose dysfunction and metabolic disease pathogenesis.

Indexed as

AdipocytesImmunity, InnateSignal TransductionAnimalscGAS-STING Signaling PathwayHumansInnate Immunity RecognitionObesityToll-Like ReceptorsToll-Like ReceptorsadipocytecGAS-STINGinnate immunityobesityToll-like receptors

Identifiers

PMID41717842
PMCPMC12987716

What Socratic holds

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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 Socratic graph.