ArticleFrontiers in immunology2024
Spinal HMGB1 participates in the early stages of paclitaxel-induced neuropathic pain via microglial TLR4 and RAGE activation.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 25 citations in OpenAlex.
- A critical role for α7 nicotinic acetylcholine receptor signaling in myeloid lineage cells in chronic neuropathic and inflammatory pain responses.The journal of pain · 2026Article
- HMGB1 aggravates neuronal ferroptosis and microglial inflammation in metabolic syndrome-associated cognitive impairment via the NRF2-autophagic flux axis.Molecular biomedicine · 2026Article
- Gut Microbiota Dysbiosis and CIPN: State-of-the-Art Evidence and a Microbiota-Ozone Therapeutic Framework.Cancers · 2026Review
- Prophylactic Effect of Echinacoside on PIPN by Inhibiting Spinal Neuroinflammation and Exerting Neuroprotective Effects.Physiological research · 2026Article
- Inflachromene Blocks Neuronal HMGB1 Translocation to Mitigate Hippocampal TLR4-NF-κB-Mediated Neuroinflammation and Depression-Like Behavior After Spinal Cord Injury.Molecular neurobiology · 2026Article
- Mechanistic investigation of HMGB1 in an in vitro model of the trigeminovascular system under migraine-like conditions.The journal of headache and pain · 2026Article
- Chemotherapy-derived DAMPs drive reprogramming of tumor-associated macrophages toward a pro-inflammatory phenotype in hepatocellular carcinoma.Scientific reports · 2026Article
- Review
- Microglia-derived neuroinflammatory pathways in neuropathic pain.The Korean journal of pain · 2026Review
- Effect of Chang'an decoction on ulcerative colitis by regulating T helper 17 cells and regulatory T cellsRab27 in the p53/high mobility group box 1 pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- Paclitaxel-induced neuroinflammation after systemic administration in male and female mice.The journal of pain · 2025Article
- Unraveling the Mechanisms of Madecassoside Derivatives in Wound Healing: Network Pharmacology and Experimental Validation.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Emerging targets and translational challenges in treating paclitaxel-induced peripheral neuropathy.Molecular biology reports · 2025Review
- Astrocyte elevated gene-1 (AEG-1) in myeloid cells is a key driver for the development of chemotherapy-induced peripheral neuropathy.Brain, behavior, and immunity · 2025Article
- Paclitaxel, interferons and functional reprogramming of tumor-associated macrophages in optimized chemo-immunotherapy.Journal for immunotherapy of cancer · 2025Review
- Accumulation of advanced oxidative protein products exacerbate satellite glial cells activation and neuropathic pain.Molecular medicine (Cambridge, Mass.) · 2025Article
- The role of glial cells in neuralgia: a bibliometric exploration.Frontiers in neurology · 2025Article
- Evaluation and application analysis of animal models of PIPNP based on data mining.Open life sciences · 2025Review
- TLR-4: a promising target for chemotherapy-induced peripheral neuropathy.Molecular biology reports · 2024Review
- Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Chemotherapy-induced neuropathic pain (CINP) is one of the main adverse effects of chemotherapy treatment. At the spinal level, CINP modulation involves glial cells that upregulate Toll-like receptor 4 (TLR4) and signaling pathways, which can be activated by pro-inflammatory mediators as the high mobility group box-1 (HMGB1). Objective: To evaluate the spinal role of HMGB1 in the paclitaxel-induced neuropathic pain via receptor for advanced glycation end products (RAGE) and TLR4 activation expressed in glial cells. Methods: Male C57BL/6 Wild type and TLR4 deficient mice were used in the paclitaxel-induced neuropathic pain model. The nociceptive threshold was measured using the von Frey filament test. In addition, recombinant HMGB1 was intrathecally (i.t.) injected to confirm its nociceptive potential. To evaluate the spinal participation of RAGE, TLR4, NF-kB, microglia, astrocytes, and MAPK p38 in HMGB1-mediated nociceptive effect during neuropathic pain and recombinant HMGB1-induced nociception, the drugs FPS-ZM1, LPS-RS, PDTC, minocycline, fluorocitrate, and SML0543 were respectively administrated by i.t. rout. Microglia, astrocytes, glial cells, RAGE, and TLR4 protein expression were analyzed by Western blot. ELISA immunoassay was also used to assess HMGB1, IL-1β, and TNF-α spinal levels. Results: The pharmacological experiments demonstrated that spinal RAGE, TLR4, microglia, astrocytes, as well as MAPK p38 and NF-kB signaling are involved with HMGB1-induced nociception and paclitaxel-induced neuropathic pain. Furthermore, HMGB1 spinal levels were increased during the early stages of neuropathic pain and associated with RAGE, TLR4 and microglial activation. RAGE and TLR4 blockade decreased spinal levels of pro-inflammatory cytokines during neuropathic pain. Conclusion: Taken together, our findings indicate that HMGB1 may be released during the early stages of paclitaxel-induced neuropathic pain. This molecule activates RAGE and TLR4 receptors in spinal microglia, upregulating pro-inflammatory cytokines that may contribute to neuropathic pain.
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