Evidence mapPaperPMID 35304484Full record

ArticleScientific reports2022

Transcriptomic analysis of human sensory neurons in painful diabetic neuropathy reveals inflammation and neuronal loss.

Bradford E Hall, Emma Macdonald, Margaret Cassidy, Sijung Yun, Matthew R Sapio, Pradipta Ray, Megan Doty, Pranavi Nara, Michael D Burton, Stephanie Shiers and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
9.6field-weighted citation impact, top 1% 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

54 citing papers in PubMed, 91 citations in OpenAlex.

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  8. Glucagon-Like Peptide-1 Targets in the Human Nodose Ganglion.The Journal of comparative neurology · 2026
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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

15 authors at 4 institutions in 1 country.

Bradford E HallFunctional Genomics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Drive, Room 130, Bethesda, MD, 20892, USA.
Emma Macdonald *Functional Genomics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Drive, Room 130, Bethesda, MD, 20892, USA.
Margaret Cassidy *Functional Genomics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Drive, Room 130, Bethesda, MD, 20892, USA.
Sijung YunYotta Biomed, LLC, Bethesda, MD, 20814, USA.
Matthew R SapioDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA.
Pradipta RayDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, 75080, USA.
Megan DotyFunctional Genomics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Drive, Room 130, Bethesda, MD, 20892, USA.
Pranavi NaraDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA.
Michael D BurtonNeuroimmunology and Behavior Group, School of Behavior and Brain Sciences, University of Texas at Dallas, Richardson, TX, 75080, USA.
Stephanie ShiersDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, 75080, USA.
Abhik Ray-ChaudhurySurgical Neurology Branch, Disorders and Stroke, National Institute of Neurological, National Institutes of Health, Bethesda, MD, 20892, USA.
Andrew J MannesDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA.
Theodore J PriceDepartment of Neuroscience and Center for Advanced Pain Studies, University of Texas at Dallas, Richardson, TX, 75080, USA.
Michael J IadarolaDepartment of Perioperative Medicine, Clinical Center, National Institutes of Health, Bethesda, MD, 20892, USA.
Ashok B KulkarniFunctional Genomics Section, National Institute of Dental and Craniofacial Research, National Institutes of Health, 30 Convent Drive, Room 130, Bethesda, MD, 20892, USA. ashok.kulkarni@nih.gov.
National Institutes of Health Clinical Center · USThe University of Texas at Dallas · USNational Institute of Dental and Craniofacial Research · USNational Institutes of Health · US

Funding

Characterization of Molecular Pathways in Chronic Pain ConditionsZIADE000664 · NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH · 2025 to 2025
$1.1M
Integrative And Molecular Studies Of Pain And Pain ControlZIACL090033 · CLINICAL CENTER · 2025 to 2025
$0k
The Pain Neural TranscriptomeZIACL090035 · CLINICAL CENTER · 2025 to 2025
$0k
PHOSPHORYLATION OF NEURONAL CYTOSKELETON IN NEURODEGENERATIVE DISEASESZ01DE000664 · DENTAL &CRANIOFACIAL RESEARCH · 1996 to 2005
Intramural NIH HHS Z01 DE000664Intramural NIH HHS ZIA CL090033Intramural NIH HHS ZIA CL090035Intramural NIH HHS ZIA DE000664NINDS NIH HHS R01 NS111929
6 · The paper itself

Abstract

Pathological sensations caused by peripheral painful neuropathy occurring in Type 2 diabetes mellitus (T2DM) are often described as 'sharp' and 'burning' and are commonly spontaneous in origin. Proposed etiologies implicate dysfunction of nociceptive sensory neurons in dorsal root ganglia (DRG) induced by generation of reactive oxygen species, microvascular defects, and ongoing axonal degeneration and regeneration. To investigate the molecular mechanisms contributing to diabetic pain, DRGs were acquired postmortem from patients who had been experiencing painful diabetic peripheral neuropathy (DPN) and subjected to transcriptome analyses to identify genes contributing to pathological processes and neuropathic pain. DPN occurs in distal extremities resulting in the characteristic "glove and stocking" pattern. Accordingly, the L4 and L5 DRGs, which contain the perikarya of primary afferent neurons innervating the foot, were analyzed from five DPN patients and compared with seven controls. Transcriptome analyses identified 844 differentially expressed genes. We observed increases in levels of inflammation-associated transcripts from macrophages in DPN patients that may contribute to pain hypersensitivity and, conversely, there were frequent decreases in neuronally-related genes. The elevated inflammatory gene profile and the accompanying downregulation of multiple neuronal genes provide new insights into intraganglionic pathology and mechanisms causing neuropathic pain in DPN patients with T2DM.

Indexed as

Diabetes Mellitus, Type 2Diabetic NeuropathiesNeuralgiaGanglia, SpinalGene Expression ProfilingHumansInflammationSensory Receptor CellsTranscriptome

Identifiers

PMID35304484
PMCPMC8933403
OpenAlexW4225261456

What Socratic holds

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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 Socratic graph.