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Review
. 2024 Oct 8;25(19):10785.
doi: 10.3390/ijms251910785.

Unveiling the Role of Schwann Cell Plasticity in the Pathogenesis of Diabetic Peripheral Neuropathy

Affiliations
Review

Unveiling the Role of Schwann Cell Plasticity in the Pathogenesis of Diabetic Peripheral Neuropathy

Nurul Husna Abd Razak et al. Int J Mol Sci. .

Abstract

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.

Keywords: Schwan cell plasticity; diabetic peripheral neuropathy (DPN); neurodegenerative disease.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Summary of the pathogenic mechanism in Schwann cells under diabetic conditions. Created with BioRender.com.
Figure 2
Figure 2
The organization of Remak Schwann cells and myelinating Schwann cells in peripheral nerves. Created with BioRender.com.
Figure 3
Figure 3
The role of Schwann cell plasticity in nerve regeneration. Following injury, both myelinating and Remak Schwann cells can reversibly transform into Repair Schwann cells due to the plasticity of Schwann cell phenotype. Repair Schwann cells facilitate peripheral nerve regeneration by forming the band of Bungner (1), elevating release of neurotrophic (2) and inflammatory factors (3) and promoting myelinophagy (4). Created with BioRender.com.

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