Fig. 2.
Proposed model for the mechanism by which microRNAs (miRNAs) contribute to chronic inflammatory and neuropathic pain. After peripheral inflammation or nerve injury, the increase in inflammatory mediators such as interleukin (IL)-1β causes a change in the expression of miRNAs in dorsal root ganglion (DRG) neurons. This change includes up-regulation of some miRNAs (e.g., miR-7a) and down-regulation of other miRNAs (e.g., miR-21), resulting in an alteration in pain-related genes, such as an increase in β-subunit of voltage-gated sodium channels (Nav), in DRG. Such an alteration leads to an increase in DRG neuronal excitability, spinal central sensitization, and pain hypersensitivity (hyperalgesia and allodynia).