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Diabetic peripheral neuropathy (DPN) is a prevalent complication of diabetes that affects a significant proportion of diabetic patients worldwide. Although the pathogenesis of DPN involves axonal atrophy and demyelination, the exact mechanisms remain elusive. Current research has predominantly focused on neuronal damage, overlooking the potential contributions of Schwann cells, which are the predominant glial cells in the peripheral nervous system. Schwann cells play a critical role in neurodevelopment, neurophysiology, and nerve regeneration. This review highlights the emerging understanding of the involvement of Schwann cells in DPN pathogenesis. This review explores the potential role of Schwann cell plasticity as an underlying cellular and molecular mechanism in the development of DPN. Understanding the interplay between Schwann cell plasticity and diabetes could reveal novel strategies for the treatment and management of DPN.

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, marked by Schwann cell dysfunction, demyelination, and impaired nerve regeneration. Although Schwann cells undergo phenotypic changes under hyperglycemic conditions, the underlying molecular mechanisms remain unclear. This study aimed to examine the effects of high glucose on Schwann cell phenotype and assess the involvement of the mTOR signaling pathway. Primary Schwann cells were isolated from rat sciatic nerves and cultured in media containing 5 mM (control), 25 mM, or 50 mM glucose for five days. Immunofluorescence staining and corrected total cell fluorescence (CTCF) analysis were used to evaluate expression of key markers: c-Jun, Krox-20, p75NTR, MBP, mTOR, phosphorylated mTOR (Ser2448), and AKR1B1. Among these, significant changes were observed in MBP (p = 0.002), total mTOR (p = 0.001), and phosphorylated mTOR (Ser2448) (p = 0.0179), indicating impaired mTOR activation and loss of myelin protein expression. Non-significant changes in the other markers are discussed as preliminary observations. These findings highlight mTOR dysregulation and impaired myelin protein expression as central features of Schwann cell responses to hyperglycemia, which may contribute to the development of DPN.