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April 19, 2026Neurobiology of Disease0 citationsOpen Access

Neuronal ACVR1-mediated H3K18 lactylation drives NLRP3 pyroptosis to sustain neuropathic pain via metabolic-epigenetic coupling

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XZXiaowei ZhaoXZX. ZhangYLYaqian Li

Key Points

  • The central aim is to investigate how ACVR1-mediated H3K18 lactylation contributes to NLRP3 pyroptosis and neuropathic pain.
  • Examined the role of ACVR1 in glycolysis and lactate production.
  • Analyzed the effects of H3K18 lactylation on NLRP3 activation and pyroptosis in neurons.
  • Utilized pharmacological blockade of ACVR1 and lactylation to assess pain reversal in models.
  • Evidence shows that ACVR1 promotes glycolysis, leading to increased H3K18 lactylation.
  • Activation of NLRP3 pyroptosis was linked to the sustained experience of neuropathic pain.
  • Pharmacological interventions effectively reduced established neuropathic pain symptoms.

Abstract

ACVR1-driven glycolysis promotes lactate-dependent H3K18la that activates neuronal NLRP3 pyroptosis to sustain neuropathic pain. Pharmacological blockade of ACVR1 or lactylation reverses established pain, positioning this immunometabolic axis as a tractable therapeutic target.

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Cite This Study

Zhao et al. (2026) studied this question.

synapsesocial.com/papers/69e4702d010ef96374d8d6c1https://doi.org/10.1016/j.nbd.2026.107397
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