Evidence map›Paper›PMID 35346352›Full record

ArticleClinical epigenetics2022

Epigenome-wide DNA methylation profiling of conditioned pain modulation in individuals with non-specific chronic low back pain.

Burel R Goodin, Demario S Overstreet, Terence M Penn, Rahm Bakshi, Tammie L Quinn, Andrew Sims, Travis Ptacek, Pamela Jackson, D Leann Long, Edwin N Aroke

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Clinical epigenetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
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  9. Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024
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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

10 authors at 1 institution in 1 country.

Burel R GoodinDepartment of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.
Demario S OverstreetDepartment of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.
Terence M PennDepartment of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0001-9262-2584
Rahm BakshiDepartment of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.
Tammie L QuinnDepartment of Psychology, College of Arts and Sciences, University of Alabama at Birmingham, Birmingham, AL, USA.
Andrew SimsDepartment of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.
Travis PtacekCenter for Clinical and Translational Science, University of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0002-4949-0149
Pamela JacksonDepartment of Acute, Chronic and Continuing Care, School of Nursing, University of Alabama at Birmingham, 1701 University Boulevard, Birmingham, AL, 35294, USA.
D Leann LongDepartment of Biostatistics, School of Public Health, University of Alabama at Birmingham, Birmingham, AL, USA.ORCID 0000-0001-8614-7190
Edwin N ArokeDepartment of Acute, Chronic and Continuing Care, School of Nursing, University of Alabama at Birmingham, 1701 University Boulevard, Birmingham, AL, 35294, USA. earoke@uab.edu.ORCID 0000-0002-8355-0870
University of Alabama at Birmingham · US

Funding

National Dissemination of I-Corps@NCATS: Accelerating Translation through CommercializationUL1TR003096 · NCATS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GUTIERREZ, ORLANDO M, KIMBERLY, ROBERT P. · 2019 to 2023
$43.6M
UAB Health Services Research (HSR) Training ProgramT32HS013852 · AHRQ · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LEVITAN, EMILY B, MUGAVERO, MICHAEL J · 2003 to 2024
$8.0M
Racial and Socioeconomic Differences in Chronic Low Back PainR01MD010441 · NIMHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GOODIN, BUREL R., SORGE, ROBERT · 2017 to 2021
$2.6M
Epigenomic and Gene Expression Signatures of Racial Differences in Chronic Low Back PainR01AR079178 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AROKE, EDWIN NGOMUEH · 2021 to 2024
$1.6M
AHRQ HHS T32 HS013852NCATS NIH HHS UL1 TR003096NIAMS NIH HHS R01 AR079178NIMHD NIH HHS R01 MD010441
6 · The paper itself

Abstract

backgroundThe pathoanatomic cause of chronic low back pain (cLBP) cannot be identified for up to 90% of individuals. However, dysfunctional processing of endogenous nociceptive input, measured as conditioned pain modulation (CPM), has been associated with cLBP and may involve changes in neuronal gene expression. Epigenetic-induced changes such as DNA methylation (DNAm) have been associated with cLBP.

methodsIn the present study, the relationship between CPM and DNAm changes in a sample of community-dwelling adults with nonspecific cLBP (n = 48) and pain-free controls (PFC; n = 50) was examined using reduced representation bisulfite sequencing. Gene ontology (GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were applied to identify key pathways involved in efficient versus deficient CPM.

resultsBased on CPM efficiency, we identified 6006 and 18,305 differentially methylated CpG sites (DMCs) with q values < 0.01 among individuals with cLBP and PFCs, respectively. Most of the DMCs were hypomethylated and annotated to genes of relevance to pain, including OPRM1, ADRB2, CACNA2D3, GNA12, LPL, NAXD, and ASPHD1. In both cLBP and PFC groups, the DMCs annotated genes enriched many GO terms relevant to pain processing, including transcription regulation by RNA polymerase II, nervous system development, generation of neurons, neuron differentiation, and neurogenesis. Both groups also enriched the pathways involved in Rap1-signaling, cancer, and dopaminergic neurogenesis. However, MAPK-Ras signaling pathways were enriched in the cLBP, not the PFC group.

conclusionsThis is the first study to investigate the genome-scale DNA methylation profiles of CPM phenotype in adults with cLBP and PFCs. Based on CPM efficiency, fewer DMC enrichment pathways were unique to the cLBP than the PFCs group. Our results suggest that epigenetically induced modification of neuronal development/differentiation pathways may affect CPM efficiency, suggesting novel potential therapeutic targets for central sensitization. However, CPM efficiency and the experience of nonspecific cLBP may be independent. Further mechanistic studies are required to confirm the relationship between CPM, central sensitization, and nonspecific cLBP.

Indexed as

Low Back PainDNA MethylationEpigenesis, GeneticEpigenomeHumansSequence Analysis, DNACentral sensitizationConditioned pain modulationDNA methylationEpigeneticsNonspecific chronic low back painReduced representation bisulfite sequencingRRBS

Identifiers

PMID35346352
PMCPMC8962463
OpenAlexW4220980421

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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 OpenQuestion graph.