Evidence map›Paper›PMID 31145897›Full record

ArticleExperimental neurology2019

Toll-like receptors and inflammation in metabolic neuropathy; a role in early versus late disease?

S Elzinga, B J Murdock, K Guo, J M Hayes, M A Tabbey, J Hur, E L Feldman

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 51 citations in OpenAlex.

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  15. HMGB1/TLR4 signaling pathway enhances abdominal aortic aneurysm progression in mice by upregulating necroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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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

7 authors at 2 institutions in 1 country.

S ElzingaDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
B J MurdockDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
K GuoDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA.
J M HayesDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
M A TabbeyDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
J HurDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58202, USA.
E L FeldmanDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA. Electronic address: efeldman@med.umich.edu.
University of Michigan–Ann Arbor · USUniversity of North Dakota · US

Funding

Integrated Systems Biology Approach to Diabetic Microvascular ComplicationsR24DK082841 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, BROSIUS, FRANK C · 2008 to 2020
$13.1M
Multidisciplinary Training Program in Basic Diabetes ResearchT32DK101357 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PETER ARVAN, Ormond A MacDougald · 2014 to 2026
$4.1M
Linking Nerve Bioenergetics with Metabolomics: New Insights into Diabetic NeuroapthyR21NS102924 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FELDMAN, EVA LUCILLE · 2018 to 2019
$429k
NIDDK NIH HHS R24 DK082841NIDDK NIH HHS T32 DK101357NINDS NIH HHS R21 NS102924
6 · The paper itself

Abstract

Neuropathy is a common, morbid complication of the metabolic syndrome, prediabetes, and diabetes. Recent studies have indicated a potential role for the immune system in the development of neuropathy. In particular, toll-like receptors (TLR) 2 and 4 have been linked to metabolic dysfunction, and blocking TLR4 is proposed as a treatment for neuropathic pain. In the current study, we investigated the role of the immune system, particularly TLRs 2 and 4, in the pathogenesis and progression of neuropathy. Sural or sciatic nerve gene expression arrays from humans and murine neuropathy models of prediabetes and diabetes were first analyzed to identify differentially expressed TLR2- and TLR4-associated genes within the KEGG (Kyoto Encyclopedia of Genes and Genomes) database. We observed that genes associated with TLRs 2 and 4, particularly lipopolysaccharide binding protein (LPB) and phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta (PIK3CB), were dysregulated across species and across multiple murine models of prediabetic and diabetic neuropathy. To further understand the role of these pathways in vivo, TLR 2 and 4 global knockout mice placed on a 60% high fat diet (HFD-TLR2/4

Indexed as

AnimalsDiabetic NeuropathiesDiet, High-FatHumansInflammationMetabolic SyndromeMiceToll-Like Receptor 2Toll-Like Receptor 4Toll-Like Receptor 2Toll-Like Receptor 4High fat dietPeripheral neuropathyToll-like receptor 2 and 4

Identifiers

PMID31145897
PMCPMC6708507
OpenAlexW2947151953

What OpenQuestion 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 OpenQuestion graph.