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. 2021 Aug 11;12:698249. doi: 10.3389/fimmu.2021.698249

Figure 10.

Figure 10

Mechanism of neutrophil extracellular traps (NETs) exacerbates secondary injury after spinal cord injury. Infiltrated neutrophils produce NETs, which subsequently promote neuroinflammation and blood–spinal cord barrier disruption to aggravate spinal cord edema and neuronal apoptosis partly via elevating transient receptor potential vanilloid type 4 (TRPV4) level following SCI in rats. Both inhibition of NETs formation by peptidylarginine deiminase 4 (PAD4) inhibitor and disruption of NETs by DNase 1 alleviate secondary damage and promote functional recovery after SCI.