On 29 December 2025, Prof. Ru-Rong Ji, the William Maixner Professor of Anesthesiology and Director of the Center for Translational Pain Medicine at Duke Medical Center, delivered a seminar at City University of Hong Kong entitled “Neuroglial Network in Pain.”
In his lecture, Prof. Ji presented work identifying Gpr37l1, through single‑cell analysis, as a selective G‑protein‑coupled receptor (GPCR) marker for spinal cord astrocytes that plays a beneficial role in pain resolution. Under the neuropathic pain condition, Gpr37l1‑ astrocytes were found to be deficient. Conversely, activation of GPR37L1 by maresin 1 enhanced astrocytic glutamate transporter 1 (GLT‑1) activity, reduced spinal excitatory postsynaptic currents, and reversed established neuropathic pain. This research highlights a protective astrocyte population within the dorsal spinal cord.
Prof. Ji further expanded on neuro‑glial interactions in pain pathogenesis, presenting striking findings on mitochondrial transfer from glia to neurons. His work addresses a key question in the field: how a single sensory neuron can generate and maintain sufficient mitochondria to support its activity and axonal regeneration. The study demonstrates that satellite glial cells (SGCs) that envelop sensory neurons in the dorsal root ganglion (DRG) transfer mitochondria to sensory neurons via tunnelling nanotubes in both mice and humans. This process is regulated by SGC‑derived myosin‑10 (MYO10). Deficits in mitochondrial transfer lead to nerve degeneration and neuropathic pain.
Clinically, SGCs from diabetic patients show reduced MYO10 expression and impaired mitochondrial transfer to neurons. Adoptive transfer of human SGCs into mouse DRG provided MYO10‑dependent protection against peripheral neuropathy. Prof. Ji’s research uncovers a previously unrecognised role of peripheral glia and offers new insights into small‑fibre neuropathy in diabetes, pointing toward novel therapeutic strategies for neuropathic pain management.