ArticleMolecular pain
Spinal HDAC6 mediates nociceptive behaviors induced by chronic constriction injury via neuronal activation and neuroinflammation.
Article in Molecular pain. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Pyroptosis in Peripheral Neuropathy: From Molecular Mechanisms to Therapeutic Targeting.CNS neuroscience & therapeutics · 2026Pooled it
- Microtubule Cytoskeleton Dysfunction in Chronic Pain: Mechanisms of Transport Failure and Emerging Therapeutic Targets.International journal of molecular sciences · 2026Review
- Review
- Delivery of Nerve Growth Factor via Exosome Attenuates Neuropathic Pain in a Rat Model of Chronic Constriction Injury.Current neuropharmacology · 2026Article
- New pharmacological agents and emerging therapeutic targets for painful diabetic neuropathy.Frontiers in endocrinology · 2026Review
- Histone deacetylases: the critical enzymes for microglial activation involved in neuropathic pain.Frontiers in pharmacology · 2025Review
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain (NP) is often accompanied by psychiatric comorbidities and currently lacks effective treatment. Prior research has shown that HDAC6 plays a crucial role in pain sensitization, but the specific mechanisms remain unclear. HDAC6 inhibitors have been found to alleviate mechanical allodynia caused by inflammation and peripheral nerve damage. In this study, we investigated the cellular mechanisms of HDAC6 in the development and maintenance of neuropathic pain. Our findings indicate that HDAC6 expression in the spinal cord (SC) is upregulated in a time-dependent manner following chronic constriction injury (CCI). HDAC6 is primarily expressed in neurons and microglia in the spinal cord. CCI-induced HDAC6 production was abolished by intrathecal injection of a microglia inhibitor. ACY-1215, a specific HDAC6 inhibitor, significantly reduced CCI-induced mechanical allodynia, but not thermal hyperalgesia. ACY-1215 also inhibited neuron activation and suppressed CCI-induced pyroptosis and neuroinflammatory responses. In summary, our results suggest that HDAC6 contributes to the development and maintenance of NP through neuronal activation and neuroinflammation. HDAC6 may be a promising target for treating NP.
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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.