KCNJ10 and diabetic neuropathy: In animal models of diabetic neuropathy, SGCs exhibit significant activation features, including upregulated expression of glial fibrillary acidic protein (GFAP), increased gap junction coupling between SGCs and between SGCs and neurons, heightened sensitivity to adenosine triphosphate (ATP), downregulation of potassium ion channel Kir4.1, and increased synthesis and release of pro-inflammatory cytokines.