ArticleThe Journal of clinical investigation2023
Silencing miR-21-5p in sensory neurons reverses neuropathic allodynia via activation of TGF-β-related pathway in macrophages.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Research hotspots and emerging trends of macrophages in peripheral nerve injury: a bibliometric and visualization analysis.Frontiers in cellular neuroscience · 2026Pooled it
- TRPM2 is a direct pain transducer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- TGF-β1 modulates PFC glial cell activation to facilitate exercise-induced analgesia in mice with spared nerve injury.IBRO neuroscience reports · 2026Article
- DNA Hypomethylation ofInternational journal of molecular sciences · 2026Article
- Review
- Neuropathic Pain: Mapping the miRNA Landscape.Non-coding RNA · 2026Review
- Plasma-derived exosomal miR-144-3p targeting IL-1β is involved in pressure pain threshold regulation at PC6 acupoint in myocardial ischemia rats.Journal of traditional and complementary medicine · 2026Article
- Electroacupuncture alleviates central post-stroke pain in rats by modulating miR-21-5p/TGF-β/Smads pathway.The journal of headache and pain · 2025Article
- Transferrin-phosphatidylserine liposomes target TDP-43 and neuroinflammation in male mice with neuropathic pain.Nature communications · 2025Article
- Identification of Neurotrophic Factor Related Biomarkers and Mechanistic Insights into Neuropathic Pain via Integrated Bioinformatics Analysis.ACS omega · 2025Article
- Roles of noncoding RNAs in neuropathic pain.Pain reports · 2025Review
- Role of transforming growth factorβ in neurovascular unit during cerebral small vessel disease.Fluids and barriers of the CNS · 2025Review
- The role of exosomes in immunopathology and potential therapeutic implications.Cellular & molecular immunology · 2025Review
- Role of ncRNAs in the Development of Chronic Pain.Non-coding RNA · 2025Review
- Mechanisms and Therapeutic Strategies of Macrophage Polarization in Intervertebral Disc Degeneration.JOR spine · 2025Review
- Pancreatic MicroRNAs inBiomolecules · 2025Article
- Sildenafil promotes osteogenic differentiation of human mesenchymal stem cells and inhibits bone loss by affecting the TGF-β signaling pathway.Stem cell research & therapy · 2025Article
- Emerging role of macrophages in neuropathic pain.Journal of orthopaedic translation · 2025Review
- Macrophage to neuron communication via extracellular vesicles in neuropathic pain conditions.Heliyon · 2025Article
- Dorsal root ganglion toxicity after AAV intra-CSF delivery of a RNAi expression construct into non-human primates and mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Neuropathic pain remains poorly managed by current therapies, highlighting the need to improve our knowledge of chronic pain mechanisms. In neuropathic pain models, dorsal root ganglia (DRG) nociceptive neurons transfer miR-21 packaged in extracellular vesicles to macrophages that promote a proinflammatory phenotype and contribute to allodynia. Here we show that miR-21 conditional deletion in DRG neurons was coupled with lack of upregulation of chemokine CCL2 after nerve injury and reduced accumulation of CCR2-expressing macrophages, which showed TGF-β-related pathway activation and acquired an M2-like antinociceptive phenotype. Indeed, neuropathic allodynia was attenuated after conditional knockout of miR-21 and restored by TGF-βR inhibitor (SB431542) administration. Since TGF-βR2 and TGF-β1 are known miR-21 targets, we suggest that miR-21 transfer from injured neurons to macrophages maintains a proinflammatory phenotype via suppression of such an antiinflammatory pathway. These data support miR-21 inhibition as a possible approach to maintain polarization of DRG macrophages at an M2-like state and attenuate neuropathic pain.
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Registered trials
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.