Neuropathic pain, which is intolerable and persistent, arises as a direct consequence of a lesion or disease affecting the somatosensory system and can be debilitating for the affected patients. Accumulating evidence from animal studies has revealed the potential molecular basis for
neuropathic pain, resulting in many promising therapeutic targets. While efforts at
drug discovery have been made, conventional
pharmacotherapy, including the use of
opioid analgesics, is still insufficient for the relief of
neuropathic pain. Therefore, novel target molecules that may lead to the development of promising
analgesics are eagerly anticipated for improved treatment of
neuropathic pain. In various insults such as
sepsis and
ischemia, high-mobility group box 1 (
HMGB1) is released extracellularly to induce
inflammation.
HMGB1 was originally identified as a ubiquitous
nuclear protein, but emerging evidence has suggested that
HMGB1 also plays a role in
neuroinflammation as a pro-inflammatory mediator. These findings suggest that
HMGB1 may be involved in the pathology of
neuropathic pain. In fact, some reports demonstrate an involvement of
HMGB1 in the development and maintenance of
neuropathic pain in experimental animals. Here, we overview the characteristics of
HMGB1 as a pro-inflammatory mediator and show the promise of
HMGB1 as a therapeutic target for
neuropathic pain.