Research progress of targeting NLRP3 inflammasome in peripheral nerve injury and pain

•It focuses on summarizing the regulatory mechanisms of NLRP3 inflammasome in peripheral nerve injury and nerve pain.•The excessive activation of NLRP3 inflammasome exacerbates nerve injury and nerve pain.•There may be CXCL12-CXCR4 autocrine pathway in schwann cells that regulates the activation of NLRP3 inflammasome through some intracellular signaling molecules and participates in the peripheral neuroinflammatory response.•The NLRP3 inflammasome in schwann cells affects the polarization of macrophages. Nerve injury and nerve pain are common diseases caused by neuroinflammation. Numerous studies have shown that the activation of NLRP3 (nod-like receptor family, pyrin domain-containing 3) inflammasome is involved in a various inflammatory response, such as Alzheimer's disease, diabetes, nerve damage and other diseases. The NLRP3 inflammasome is a complex containing NLRP3 protein, ASC (apoptosis-associated speckle-like protein), and pro-caspase-1, which is highly expressed and activated to promote the secretion of IL-1β and IL-18 in response to the stimulation of danger-associated molecular patterns (DAMPs) and pathogen-associated molecular patterns (PAMPs) in immune cells such as macrophages and dendritic cells. The activation of NLRP3 inflammasome can cause cell death through caspase-1-mediated cell pyroptosis and plays an important role in the development of nervous system injury and inflammation-related diseases. This discussion aims to summarize the mechanisms of nerve damage and pain caused by excessive activation of the NLRP3 inflammasome.