ArticleClinical epigenetics2022
Epigenome-wide DNA methylation profiling of conditioned pain modulation in individuals with non-specific chronic low back pain.
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.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Epigenetic Factors Related to Low Back Pain: A Systematic Review of the Current Literature.International journal of molecular sciences · 2023Pooled it
- MicroRNA-148a regulates depressive-like behaviors in mice via the Otx2/Dopaminergic signaling axis.Molecular psychiatry · 2026Article
- Rap1-Dependent pathways in depression: Genetic, Epigenetic, and neuroinflammatory mechanisms shaping synaptic resilience.Molecular biology reports · 2025Review
- Review
- Investigating the epigenetic landscape of symptomatic disk degeneration: a case study.Pain reports · 2025Article
- Unveiling the Mechanisms of Pain in Endometriosis: Comprehensive Analysis of Inflammatory Sensitization and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Impaired Molecular Mechanisms Contributing to Chronic Pain in Patients with Hidradenitis Suppurativa: Exploring Potential Biomarkers and Therapeutic Targets.International journal of molecular sciences · 2025Article
- Systemic Inflammation, Sleep, and Psychological Factors Determine Recovery Trajectories for People With Neck Pain: An Exploratory Study.The journal of pain · 2024Article
- Pathology of pain and its implications for therapeutic interventions.Signal transduction and targeted therapy · 2024Review
- The Pace of Biological Aging Predicts Nonspecific Chronic Low Back Pain Severity.The journal of pain · 2024Article
- Epigenetic Connections of the TRPA1 Ion Channel in Pain Transmission and Neurogenic Inflammation - a Therapeutic Perspective in Migraine?Molecular neurobiology · 2023Review
- Protocol for Biospecimen Collection and Analysis Within the BACPAC Research Program.Pain medicine (Malden, Mass.) · 2023Article
- Challenges in Analyzing Functional Epigenetic Data in Perspective of Adolescent Psychiatric Health.International journal of molecular sciences · 2022Review
- Genome-wide DNA methylation study identifies significant epigenomic changes associated with internalized stigma in adults with non-specific chronic low back pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Next-generation DNA methylation sequencing: loci and regions differentially methylated in adolescents with chronic postsurgical pain.Neurobiology of pain (Cambridge, Mass.)Article
- The pace of biological aging helps explain the association between insomnia and chronic low back pain.Molecular painArticle
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
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.
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