ePoster

SATELLITE GLIAL CELLS MODULATE PAIN AND NEURAL REGENERATION IN DIABETIC PERIPHERAL NEUROPATHY

Jiangwei Wu

The University of Hong Kong

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-398

Presentation

Date TBA

Board: PS02-07PM-398

Poster preview

SATELLITE GLIAL CELLS MODULATE PAIN AND NEURAL REGENERATION IN DIABETIC PERIPHERAL NEUROPATHY poster preview

Event Information

Poster Board

PS02-07PM-398

Abstract

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes and is frequently accompanied by chronic pain or, at later stages, painless but progressive neural dysfunction. While neuronal damage has been extensively studied, the contribution of peripheral glial cells to pain regulation and neural regeneration in DPN remains poorly understood. Satellite glial cells (SGCs), which closely envelop sensory neurons in dorsal root ganglia, play a critical role in maintaining neuronal homeostasis and modulating sensory signaling. In this study, we investigated the involvement of SGCs in pain-related phenotypes of DPN and explored whether exogenous supplementation of SGCs could support neural regeneration. Using a streptozotocin-induced diabetic rat model, pain sensitivity was assessed behaviorally to characterize neuropathic pain states. Peripheral nervous tissues were analyzed to evaluate glial and neuronal alterations associated with diabetes. Furthermore, exogenous SGCs were introduced to examine their potential effects on neuronal support and regenerative responses under diabetic conditions. Our findings suggest that dysfunction of SGCs is associated with altered pain processing and impaired neural repair in DPN. Importantly, supplementation with SGCs showed potential to improve the neural microenvironment, supporting neuronal integrity and regenerative capacity. These results highlight a previously underappreciated role of satellite glial cells in diabetic peripheral neuropathy and suggest that targeting peripheral glial support may represent a promising strategy for modulating pain and promoting neural regeneration in DPN.

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