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. 2022 Oct 10;18(5):996–1003. doi: 10.4103/1673-5374.355748

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Copyright: © Neural Regeneration Research

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Schematic illustration of potential mechanisms involved in the NO/cGMP signaling pathway in bone cancer pain.

Activated NMDAR receptor promotes the activation of PSD95 and nNOS, and then induces activation of the NO/cGMP/PKG-I signal pathway, which is involved in the development of bone cancer pain. MrgC induces the activation of Gi protein, which in turn reduces spinal NMDAR-NR2B and nNOS and alleviates pain behavior. CCR2 also improves the activation of NMDAR and nNOS in the spinal cord. AC: Adenylate cyclase; CCR2: chemokine C-C motif receptor 2; cGMP: cyclic guanosine 3′,5′-monophosphate; GC: guanylate cyclase; Gi protein: inhibitory guanine nucleotide regulatory proteins; MrgC: Mas oncogene-related gene C receptors; NMDAR: N-methyl-D-aspartate receptors; nNOS: neuronal NOS; NO: nitric oxide; PKG: protein kinase G; PSD95: postsynaptic density protein 95; TCI: tumor cell implantation.