Evidence map›Paper›PMID 28661198›Full record

ReviewAntioxidants & redox signaling2018

Metabolic Regulation of Adipose Tissue Macrophage Function in Obesity and Diabetes.

Mahesh Appari, Keith M Channon, Eileen McNeill

Open access · bronzeAbstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 3 pooled it
8.1field-weighted citation impact, top 2% 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

67 citing papers in PubMed, 3 syntheses or guidelines pooled it, 136 citations in OpenAlex.

  1. Pooled it
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  14. Microbial Biotransformation of Chicory byInternational journal of molecular sciences · 2025
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7 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Mahesh Appari1 Division of Cardiovascular Medicine, British Heart Foundation Centre for Research Excellence, John Radcliffe Hospital, University of Oxford , Oxford, United Kingdom .
Keith M Channon1 Division of Cardiovascular Medicine, British Heart Foundation Centre for Research Excellence, John Radcliffe Hospital, University of Oxford , Oxford, United Kingdom .
Eileen McNeill1 Division of Cardiovascular Medicine, British Heart Foundation Centre for Research Excellence, John Radcliffe Hospital, University of Oxford , Oxford, United Kingdom .
Centre for Human Genetics · GBUniversity of Oxford · GB

Funding

British Heart Foundation PG/15/35/31403British Heart Foundation RG/12/5/29576British Heart Foundation RG/15/10/31485British Heart Foundation RG/17/10/32859Medical Research Council G0200482Medical Research Council G0400144Wellcome Trust 090532/Z/09/Z
6 · The paper itself

Abstract

significanceObesity and diabetes are associated with chronic activation of inflammatory pathways that are important mechanistic links between insulin resistance (IR), type 2 diabetes (T2D), and cardiovascular disease pathogenesis. The development of these metabolic diseases is associated with changes in both the number and phenotype of adipose tissue macrophages (ATMs). Emerging lines of evidence have shown that ATMs release proinflammatory cytokines similar to classically activated M1 macrophages, which directly contribute to IR or T2D. In contrast, adipose tissue (AT) from lean healthy individuals contains macrophages with a less inflammatory M2 phenotype. Recent Advances: Recent research has shown that macrophage phenotype is linked to profound changes in macrophage cellular metabolism. CRITICAL ISSUES: This review focuses on the role of macrophages in AT inflammation and obesity, and the metabolic changes in macrophage function that occur with activation that underpin their role in the pathogenesis of IR and T2D. We highlight current targets for altering macrophage metabolism from both within the field of metabolic disease and AT biology and more widely within inflammatory biology. FUTURE DIRECTIONS: As our knowledge of macrophage metabolic programming in AT builds, there will be increasing scope for targeting this aspect of macrophage biology as a therapeutic strategy in metabolic diseases. Antioxid. Redox Signal. 29, 297-312.

Indexed as

Adipose TissueAnimalsDiabetes Mellitus, Type 2HumansMacrophagesObesitydiabetesimmunometabolismmacrophagesobesityredox signaling

Identifiers

PMID28661198
PMCPMC6012981
OpenAlexW2724411529

What OpenQuestion 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 OpenQuestion graph.