Autophagy in Schwann cells: A potential pharmacotherapeutic target in diabetic peripheral neuropathy

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Diabetic peripheral neuropathy (DPN) is a common complication of diabetes and is characterized by sensory and motor impairments resulting from neural injury. Schwann cells (SCs), which are important for peripheral nerve function, are compromised under hyperglycemic conditions, leading to impaired axonal regeneration and demyelination. Autophagy, a cellular degradation process, is essential for SC function and significantly influences DPN progression. This article highlights the significance of autophagy in SCs and its potential as a pharmacotherapeutic target in DPN. We discuss the mechanisms of autophagy in SCs, including the mammalian target of rapamycin, adenosine monophosphate-activated protein kinase, and phosphatase and tensin homolog-induced putative kinase/parkin pathways, and their dysregulation in DPN. This article also examines various natural products and chemical agents that modulate autophagy and enhance the efficacy of DPN treatment. These agents target key signaling pathways, such as adenosine monophosphate-activated protein kinase/mammalian target of rapamycin and demonstrate potential in promoting nerve regeneration and restoring SC function. The roles of exosomes, long non-coding RNA, and proteins in the regulation of autophagy have also been explored. In conclusion, targeting autophagy in SCs is a promising strategy for DPN treatment and offers new insights

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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