Evidence map›Paper›PMID 36613673›Full record

ArticleInternational journal of molecular sciences2022

Asprosin Exerts Pro-Inflammatory Effects in THP-1 Macrophages Mediated via the Toll-like Receptor 4 (TLR4) Pathway.

Kiran Shabir, Seley Gharanei, Sophie Orton, Vanlata Patel, Parbata Chauhan, Emmanouil Karteris, Harpal S Randeva, James E Brown, Ioannis Kyrou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Observational
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  4. Article
  5. Article
  6. Asprosin activates multiple placental pathwaysMolecular medicine reports · 2025
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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

9 authors at 5 institutions in 2 countries.

Kiran ShabirWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.ORCID 0000-0003-1633-1552
Seley GharaneiWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.ORCID 0000-0002-5935-8950
Sophie OrtonWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.
Vanlata PatelWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.
Parbata ChauhanAston Medical School, College of Health and Life Sciences, Aston University, Birmingham B4 7ET, UK.
Emmanouil KarterisCollege of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK.
Harpal S RandevaWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.
James E BrownAston Medical School, College of Health and Life Sciences, Aston University, Birmingham B4 7ET, UK.
Ioannis KyrouWarwick Medical School, University of Warwick, Coventry CV4 7AL, UK.ORCID 0000-0002-6997-3439
University of Warwick · GBAston University · GBUniversity Hospitals Coventry and Warwickshire NHS Trust · GBAgricultural University of Athens · GRBrunel University of London · GB

Funding

Aston University Aston University 50th Anniversary Prize PhD Student-ships SchemeUniversity Hospital Coventry UHCW NHS trust
6 · The paper itself

Abstract

Adipose tissue is a dynamic endocrine organ, secreting a plethora of adipokines which play a key role in regulating metabolic homeostasis and other physiological processes. An altered adipokine secretion profile from adipose tissue depots has been associated with obesity and related cardio-metabolic diseases. Asprosin is a recently described adipokine that is released in response to fasting and can elicit orexigenic and glucogenic effects. Circulating asprosin levels are elevated in a number of cardio-metabolic diseases, including obesity and type 2 diabetes. In vitro studies have reported pro-inflammatory effects of asprosin in a variety of tissues. The present study aimed to further elucidate the role of asprosin in inflammation by exploring its potential effect(s) in THP-1 macrophages. THP-1 monocytes were differentiated to macrophages by 48 h treatment with dihydroxyvitamin D3. Macrophages were treated with 100 nM recombinant human asprosin, 100 ng/mL lipopolysaccharide (LPS), and 10 μM caffeic acid phenethyl ester (CAPE; an inhibitor of NFκB activation) or 1 µM TAK-242 (a Toll-like receptor 4, TLR4, inhibitor). The expression and secretion of pertinent pro-inflammatory mediators were measured by qPCR, Western blot, ELISA and Bioplex. Asprosin stimulation significantly upregulated the expression and secretion of the pro-inflammatory cytokines: tumour necrosis factor α (TNFα), interleukin-1β (IL-1β), IL-8 and IL-12 in vitro. This pro-inflammatory response in THP-1 macrophages was partly attenuated by the treatments with CAPE and was significantly inhibited by TAK-242 treatment. Asprosin-induced inflammation is significantly counteracted by TLR4 inhibition in THP-1 macrophages, suggesting that asprosin exerts its pro-inflammatory effects, at least in part, via the TLR4 signalling pathway.

Indexed as

AdipokinesDiabetes Mellitus, Type 2MacrophagesToll-Like Receptor 4HumansInflammationLipopolysaccharidesSulfonamidesTHP-1 CellsAdipokinesethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateLipopolysaccharidesSulfonamidesTLR4 protein, humanToll-Like Receptor 4adipokinesasprosininflammationTHP-1 macrophagesTLR4Toll-like receptor 4

Identifiers

PMID36613673
PMCPMC9820073
OpenAlexW4312172075

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.