DNM2 and Hyperglycemia: In the pathophysiology of diabetes, the core mechanism underlying abnormal protein modification is the non-enzymatic glycation reaction resulting from chronic hyperglycemia, which culminates in the formation of advanced glycation end products by directly cross-linking with long-lived proteins in nerve tissue, such as myelin and cytoskeletal proteins, thereby disrupting their structure and function (21–23), and by binding to their specific receptor to activate downstream inflammatory and oxidative stress pathways (24).