Evidence map›Paper›PMID 28272773›Full record

ArticleJournal of cellular and molecular medicine2017

Comparative RNA-Seq transcriptome analyses reveal distinct metabolic pathways in diabetic nerve and kidney disease.

Lucy M Hinder, Meeyoung Park, Amy E Rumora, Junguk Hur, Felix Eichinger, Subramaniam Pennathur, Matthias Kretzler, Frank C Brosius, Eva L Feldman

Open access · goldAbstract readComparative Study
In one paragraph

Article in Journal of cellular and molecular medicine, 2017. 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, 56 citations in OpenAlex.

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  16. Systems Biology to Address Unmet Medical Needs in Neurological Disorders.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  17. Article
  18. Gene expression profiles of diabetic kidney disease and neuropathy in eNOS knockout mice: Predictors of pathology and RAS blockade effects.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
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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 2 institutions in 1 country.

Lucy M HinderDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
Meeyoung ParkDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
Amy E RumoraDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
Junguk HurDepartment of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND, USA.
Felix EichingerDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Subramaniam PennathurDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Matthias KretzlerDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Frank C BrosiusDepartment of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.
Eva L FeldmanDepartment of Neurology, University of Michigan, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · USUniversity of North Dakota · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
Research BaseP30DK092926 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MARY ELLEN MICHELE HEISLER, ADESUWA B OLOMU · 2011 to 2026
$10.0M
Vanderbilt Mouse Metabolic Phenotyping CenterU2CDK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2016 to 2021
$6.3M
Michigan Mouse Metabolic Phenotyping CenterU2CDK110768 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ELIAS, CAROL FUZETI · 2016 to 2021
$6.2M
Tissue-Specific Metabolic Reprogramming in Diabetic ComplicationsDP3DK094292 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BROSIUS, FRANK C, BURANT, CHARLES F · 2011 to 2011
$5.5M
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
NIDDK NIH HHS DP3 DK094292NIDDK NIH HHS P30 DK020572NIDDK NIH HHS P30 DK081943NIDDK NIH HHS P30 DK092926NIDDK NIH HHS T32 DK101357NIDDK NIH HHS U24 DK059637NIDDK NIH HHS U2C DK059637NIDDK NIH HHS U2C DK110768
6 · The paper itself

Abstract

Treating insulin resistance with pioglitazone normalizes renal function and improves small nerve fibre function and architecture; however, it does not affect large myelinated nerve fibre function in mouse models of type 2 diabetes (T2DM), indicating that pioglitazone affects the body in a tissue-specific manner. To identify distinct molecular pathways regulating diabetic peripheral neuropathy (DPN) and nephropathy (DN), as well those affected by pioglitazone, we assessed DPN and DN gene transcript expression in control and diabetic mice with or without pioglitazone treatment. Differential expression analysis and self-organizing maps were then used in parallel to analyse transcriptome data. Differential expression analysis showed that gene expression promoting cell death and the inflammatory response was reversed in the kidney glomeruli but unchanged or exacerbated in sciatic nerve by pioglitazone. Self-organizing map analysis revealed that mitochondrial dysfunction was normalized in kidney and nerve by treatment; however, conserved pathways were opposite in their directionality of regulation. Collectively, our data suggest inflammation may drive large fibre dysfunction, while mitochondrial dysfunction may drive small fibre dysfunction in T2DM. Moreover, targeting both of these pathways is likely to improve DN. This study supports growing evidence that systemic metabolic changes in T2DM are associated with distinct tissue-specific metabolic reprogramming in kidney and nerve and that these changes play a critical role in DN and small fibre DPN pathogenesis. These data also highlight the potential dangers of a 'one size fits all' approach to T2DM therapeutics, as the same drug may simultaneously alleviate one complication while exacerbating another.

Indexed as

Gene Expression ProfilingMetabolic Networks and PathwaysSequence Analysis, RNAAnimalsComputational BiologyDiabetic NephropathiesDiabetic NeuropathiesKidney GlomerulusMaleMice, Inbred C57BLNerve FibersOrgan SpecificityPioglitazoneReproducibility of ResultsRNA, MessengerThiazolidinedionesPioglitazoneRNA, MessengerThiazolidinedionesdiabetic nephropathydiabetic peripheral neuropathypioglitazonetype 2 diabetes

Identifiers

PMID28272773
PMCPMC5571536
OpenAlexW2592445753

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.