MicroRNAs in Fibromyalgia: Promising Biomarker Candidates with Implications for Pain
Fibromyalgia is a complex chronic pain syndrome with poorly understood pathophysiology and no definitive biomarker. miRNAs are post-transcriptional regulators that might contribute to mechanisms implicated in fibromyalgia, including central sensitization and immune dysregulation. Several miRNAs have been reported to be altered in patients with fibromyalgia and might be involved in inflammatory, neuronal, and metabolic pathways. Although preliminary studies suggest that miRNA profiles may help distinguish patients with fibromyalgia, findings remain heterogeneous and limited by small sample sizes and methodological variability. miRNAs represent promising candidates for interpreting fibromyalgia pathophysiology and developing minimally invasive biomarkers, although further standardized and adequately powered studies are required to establish their clinical utility. This narrative review summarizes the current evidence on miRNA dysregulation in fibromyalgia and assesses its potential relevance as a biomarker. Particular attention is given to miRNAs dysregulated in fibromyalgia that exhibit similar expression patterns in other painful conditions, with the aim of identifying shared molecular signatures associated with pain. This approach might provide insight into the biological mechanisms underlying fibromyalgia by identifying molecular alterations shared with other painful conditions, supporting its characterization as a disorder involving both chronic pain and altered tissue homeostasis.
Authors
- Eduardo Cimadevilla-Fernández-Pola (ORCID: https://orcid.org/0000-0002-8168-2845)
- Mario García‐Domínguez (ORCID: https://orcid.org/0000-0002-4263-7363)
Institutions
- Universidad Nebrija (ES)
- Universidad Alfonso X el Sabio (ES)
Publication Details
- Journal
- Genes
- Published
- 2026-10-22
- DOI
- https://doi.org/10.3390/genes17111318
- Primary Topic
- Fibromyalgia and Chronic Fatigue Syndrome Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00