Our findings demonstrated robust upregulation and activation of both PKC-α and MAPK14 within the SGs under the T2DM condition (Figure 4B,D), aligning with the role of PKC-α in SGC-mediated modulation of Ca2+ channel function, neuroinflammation, and autonomic imbalance via glial-derived factors that heighten the neuronal excitability. This evidence concerns the gene MAPK14 and type 2 diabetes mellitus.