ReviewMolecular medicine (Cambridge, Mass.)2015
Extracellular high-mobility group box 1 protein (HMGB1) as a mediator of persistent pain.
Review in Molecular medicine (Cambridge, Mass.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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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.
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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
53 citing papers in PubMed, 93 citations in OpenAlex.
- Effects of MC-100093, GLT-1 enhancer, in mesolimbic brain regions of C57BL/6 mouse exposed to hydrocodone high-dose challenge using comprehensive laboratory monitoring system.IBRO neuroscience reports · 2026Article
- Regulatory effects and mechanisms of the acupuncture-induced complement component 1q on the high mobility group box 1 -receptor for advanced glycation end products-nuclear factor kappa-B pathway at Zusanli (ST36).Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain.Bioelectronic medicine · 2026Review
- Otilonium bromide ameliorates paclitaxel-induced peripheral neuropathy by targeting phosphatase PPM1A.Journal of neuroinflammation · 2026Article
- Taxifolin Attenuates Remote Lung Injury Induced by Hepatic Ischemia-Reperfusion in Rats.Molecules (Basel, Switzerland) · 2026Article
- Thrombomodulin-Induced Prevention of Peripheral Neuropathy in Oxaliplatin-Treated Mice Involves Complement C5a Inactivation and PAR1 Activation in Addition To HMGB1 Degradation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Modulation of persistent bladder pain in mice: The role of macrophage migration inhibitory factor, high mobility group box-1, and downstream signaling pathways.Bladder (San Francisco, Calif.) · 2024Article
- Spinal HMGB1 participates in the early stages of paclitaxel-induced neuropathic pain via microglial TLR4 and RAGE activation.Frontiers in immunology · 2024Article
- Hmgb1 Silencing in the Amygdala Inhibits Pain-Related Behaviors in a Rat Model of Neuropathic Pain.International journal of molecular sciences · 2023Article
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- HMGB1 mediates synaptic loss and cognitive impairment in an animal model of sepsis-associated encephalopathy.Journal of neuroinflammation · 2023Article
- Clinical Biomarker of Sterile Inflammation, HMGB1, in Patients with Chronic Non-Specific Low Back Pain: A Pilot Cross-Sectional Study.Life (Basel, Switzerland) · 2023Article
- HMGB1 in the mPFC governs comorbid anxiety in neuropathic pain.The journal of headache and pain · 2022Article
- Expression of adipokines and adipocytokines by epidural adipose tissue in cauda equina syndrome in dogs.Journal of veterinary internal medicine · 2022Article
- Role of HMGB1 in Vitiligo: Current Perceptions and Future Perspectives.Clinical, cosmetic and investigational dermatology · 2022Review
- Bladder Oxidative Stress and HMGB1 Release Contribute to PAR4-Mediated Bladder Pain in Mice.Frontiers in systems neuroscience · 2022Article
- Article
- Review
- Sensory Neuron TLR4 mediates the development of nerve-injury induced mechanical hypersensitivity in female mice.Brain, behavior, and immunity · 2021Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although originally described as a highly conserved nuclear protein, high-mobility group box 1 protein (HMGB1) has emerged as a danger-associated molecular pattern molecule protein (DAMP) and is a mediator of innate and specific immune responses. HMGB1 is passively or actively released in response to infection, injury and cellular stress, providing chemotactic and cytokine-like functions in the extracellular environment, where it interacts with receptors such as receptor for advanced glycation end products (RAGE) and several Toll-like receptors (TLRs). Although HMGB1 was first revealed as a key mediator of sepsis, it also contributes to a number of other conditions and disease processes. Chronic pain arises as a direct consequence of injury, inflammation or diseases affecting the somatosensory system and can be devastating for the affected patients. Emerging data indicate that HMGB1 is also involved in the pathology of persistent pain. Here, we give an overview of HMGB1 as a proinflammatory mediator, focusing particularly on the role of HMGB1 in the induction and maintenance of hypersensitivity in experimental models of pain and discuss the therapeutic potential of targeting HMGB1 in conditions of chronic pain.
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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.