Targeting Fgr-STAT3 Mediated Autophagy Inhibition in the Spinal Cord Alleviates Neuropathic Pain in Rats

Fgr kinase expression increases significantly in spinal microglia following nerve damage.

• Chronic nerve injury leads to a prolonged rise in Fgr expression in microglia of the spinal dorsal horn.
• Fgr overexpression is associated with the development of pain symptoms, while Fgr knockdown may reduce pain hypersensitivity.
• Fgr phosphorylates STAT3, which may promote its movement into the nucleus and decrease the process of autophagy.
• Inhibition of Fgr with TL02-59 may restore autophagy and reduce STAT3 activation, potentially alleviating neuropathic pain behaviors.
• The Fgr-STAT3 signaling pathway could be a target for therapies aimed at improving microglial autophagy and managing neuropathic pain.

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