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Schematic hypothesis of neuronal-astrocytic CXCR4 and CX43-mediated diabetic neuropathic pain. STZ-induced type 1 diabetes resulted in persistent upregulation of CXCR4 and CX43 in astrocytes and neurons. It is shown that persistent increase of CXCR4 may cause activated neuron excitability and CX43 may mediate intercellular inflammation signal transmission, then dysfunctional astrocytes cannot counter the inflammatory factors at late phase of diabetes, and DNP occurs and exacerbates.
