Upregulation of Mlxipl induced by cJun in the spinal dorsal horn after peripheral nerve injury counteracts mechanical allodynia by inhibiting neuroinflammation

Neuropathic pain (NP) is a debilitating clinical condition caused by a lesion or disease of the somatosensory system, leading to spontaneous pain and increased sensitivity. Current treatments are unsatisfactory, highlighting the need to understand its causes. This study investigates the role of Mlxipl, a glucose-responsive transcription factor, in neuropathic pain. The research explores how Mlxipl influences inflammation in the spinal dorsal horn (SDH) following nerve injury, potentially alleviating neuropathic pain. The study reveals that after nerve injury, Mlxipl expression increases in the spinal dorsal horn. This upregulation, driven by the transcription factor cJun, appears to inhibit neuroinflammation, thus providing a protective mechanism against neuropathic pain.

• 1
  Mlxipl expression is upregulated in the ipsilateral spinal dorsal horn (SDH) of rats with Spared Nerve Injury (SNI)-induced mechanical allodynia.
• 2
  Knockdown of Mlxipl in the SDH aggravated mechanical allodynia and neuroinflammation, while overexpression of Mlxipl inhibited these effects.
• 3
  The transcription factor cJun directly promotes Mlxipl expression at the transcriptional level by binding to the Mlxipl promoter.