ArticleJournal of translational medicine2025
Regulation of macrophages in the dorsal root ganglion through TGF-β1 inhibits painful traumatic neuroma.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Dexmedetomidine Alleviates Visceral Pain by Modulating a Pro-Inflammatory Macrophage-Associated Gene Network.Biomedicines · 2026Article
- TGF-β1 Promotes the Recovery of Dorsal Root Ganglion Neurons from Cisplatin-Induced Injury Through Smad4-Dependent Mechanism.Current issues in molecular biology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundThe mechanisms underlying neuropathic pain in traumatic neuromas following peripheral nerve injury have become a major research focus in the field of pain medicine. Transforming growth factor-β1 (TGF-β1), an anti-inflammatory cytokine, is significantly elevated in the dorsal root ganglion (DRG) after peripheral nerve injury. This study investigates the role and mechanisms of TGF-β1 in traumatic neuroma formation and neuropathic pain.
methodsIn vivo, neuropathic pain-related behaviors, neuroma formation, activation of nerve fibers in the dorsal root ganglion (DRG), and macrophage polarization were evaluated in rats subjected to sciatic nerve transection (SNT) to examine whether TGF-β1 plays a role in preventing traumatic neuroma. In vitro, RAW 264.7 cells were stimulated with lipopolysaccharide (LPS) (500 ng/mL) to simulate traumatic neuroma-induced pathological changes in DRG macrophages, aiming to assess whether TGF-β1 alters the balance of macrophage polarization.
resultsIn vivo, rapamycin (RAPA) treatment effectively reduced neuroma formation and alleviated neuropathic pain in rats, whereas these therapeutic effects were reversed upon inhibition of TGF-β1. In vitro, rapamycin treatment downregulated the expression of M1-related proteins (TNF-α, iNOS, and IL-1β) while upregulating M2-related proteins (Arg1 and IL-10). These effects were largely abolished when TGF-β1 siRNA was introduced. Furthermore, supplementation with exogenous recombinant TGF-β1 again reversed the M1/M2 polarization balance.
conclusionsThese findings suggest that TGF-β reduces the M1/M2 macrophage ratio by mediating the polarization direction of macrophages within DRGs. This mechanism may block the transmission of peripheral nociceptive signals, thereby promoting the repair of nerve injury. The study provides concrete evidence to guide the development of new therapeutic strategies for painful neuroma.
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