Evidence map›Paper›PMID 41556140›Full record

ArticleThe Journal of clinical endocrinology and metabolism2026

NGF promotes, in an autocrine-paracrine manner, metabolic and anti-inflammatory pathways in human and mouse adipocytes.

Michail Deiktakis, Elias Athanasakis, Ioannis Charalampopoulos, Achille Gravanis, Christos Tsatsanis, Maria Venihaki, Andrew N Margioris, Eirini Dermitzaki

Abstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

8 authors.

Michail DeiktakisLaboratory of Clinical Chemistry, Department of Laboratory Medicine, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0009-0000-4045-374X
Elias AthanasakisDepartment of General Surgery, University Hospital of Heraklion, Heraklion 71110, Crete, Greece.ORCID 0000-0002-5508-4251
Ioannis CharalampopoulosLaboratory of Pharmacology, Department of Basic Sciences, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0000-0003-3415-7332
Achille GravanisLaboratory of Pharmacology, Department of Basic Sciences, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0000-0001-5435-1939
Christos TsatsanisLaboratory of Clinical Chemistry, Department of Laboratory Medicine, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0000-0003-1214-4151
Maria VenihakiLaboratory of Clinical Chemistry, Department of Laboratory Medicine, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0000-0002-3789-8032
Andrew N MargiorisLaboratory of Clinical Chemistry, Department of Laboratory Medicine, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.
Eirini DermitzakiLaboratory of Clinical Chemistry, Department of Laboratory Medicine, School of Medicine, University of Crete, Heraklion 71003, Crete, Greece.ORCID 0000-0002-5826-3992

Funding

University of Crete 3330
6 · The paper itself

Abstract

contextNerve growth factor (NGF) affects the development and survival of sympathetic neurons. NGF is also found in non-neural cell lineages that are implicated in immune-endocrine interactions associated with metabolic diseases. Although NGF is expressed in white adipose tissue (WAT), little is known about the regulation of its expression and role in adipocytes.

objectiveTo determine whether NGF and its receptors are expressed in human adipocytes and demonstrate their role in adipocyte metabolic and inflammatory phenotypes.

methodsThe expression of NGF and its receptors, tropomyosin-related kinase A (TrkA) and pan-neurotrophin receptor (p75NTR), and their effects on metabolic and inflammatory responses were examined in freshly isolated adipocytes from human abdominal WAT and mouse 3T3L1 cells.

resultsTrkA and p75NTR were expressed in both human and mouse adipocytes and pre-adipocytes. NGF was secreted by human white adipocytes and their exogenous exposure to NGF increased mitochondrial mass and activity, peroxisome proliferator-activated receptor gamma, CCAAT/enhancer binding protein alpha, and adiponectin levels. Additionally, NGF increased lipolysis in human WAT explants and suppressed lipids accumulation, lipoprotein lipase, and pro-inflammatory mediators interleukin (IL)-6 and IL-8 in human white adipocytes. The pro-inflammatory factor lipopolysaccharide downregulated the levels of NGF receptors in human white adipocytes. NGF also affected mitochondrial activity in both human and mouse pre-adipocytes and TrkA appeared to mediate, at least partially, the effects of NGF on adipocytes.

conclusionOur data suggest that NGF is produced locally within the adipose tissue where it upregulates mitochondrial function while it suppresses the pro-inflammatory phenotype of human and mouse adipocytes.

Indexed as

AdipocytesAutocrine CommunicationInflammationNerve Growth Factor3T3-L1 CellsAdipocytes, WhiteAdipose Tissue, WhiteAnimalsCells, CulturedHumansLipolysisMiceMitochondriaReceptors, Nerve Growth FactorReceptor, trkANerve Growth FactorReceptors, Nerve Growth FactorReceptor, trkAadipocyteinflammationmetabolismobesity

Identifiers

PMID41556140
PMCPMC13502198

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Registered trials

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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.