Evidence map›Paper›PMID 22294100›Full record

ReviewCellular and molecular life sciences : CMLS2012

A role for sphingolipids in the pathophysiology of obesity-induced inflammation.

Benjamin T Bikman

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 65 citations in OpenAlex.

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  13. Ketones Elicit Distinct Alterations in Adipose Mitochondrial Bioenergetics.International journal of molecular sciences · 2020
    Article
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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

1 author at 1 institution in 1 country.

Benjamin T BikmanDepartment of Physiology and Developmental Biology, Brigham Young University, Provo, UT 84602, USA. benjamin_bikman@byu.edu
Brigham Young University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following the initial discovery that adipose tissue actively synthesizes and secretes cytokines, obesity-induced inflammation has been implicated in the etiology of a host of disease states related to obesity, including cardiovascular disease and type II diabetes. Interestingly, a growing body of evidence similarly implicates sphingolipids as prime instigators in these same diseases. From the recent discovery that obesity-related inflammatory pathways modulate sphingolipid metabolism comes a novel perspective—sphingolipids may act as the dominant mediators of deleterious events stemming from obesity-induced inflammation. This paradigm may identify sphingolipids as an effective target for future therapeutics aimed at ameliorating diseases associated with chronic inflammation.

Indexed as

Models, BiologicalCardiovascular DiseasesCeramidesCytokinesFatty LiverHumansInflammationInsulin ResistanceNon-alcoholic Fatty Liver DiseaseObesitySignal TransductionSphingolipidsToll-Like Receptor 4CeramidesCytokinesSphingolipidsTLR4 protein, humanToll-Like Receptor 4

Identifiers

PMID22294100
PMCPMC11114706
OpenAlexW2015462643

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.