Schwann cell reprogramming via EMT-like program following peripheral nerve injury and during nerve regeneration

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)

The activation of the epithelial-mesenchymal transition (EMT) enhances cell plasticity and plays a pivotal role in driving critical biological processes such as embryonic process, tissue repair, and cancer metastasis. EMT is regulated by multiple signaling pathways, including transforming growth factor-β (TGF-β), Wnt, and Notch signaling, and is finely orchestrated by a network of transcriptional factors, epigenetic modifications (such as DNA methylation and histone alterations), and non-coding RNAs. In the peripheral nervous system, Schwann cells undergo a distinct EMT-like transformation following nerve injury, adopting a repair phenotype known as repair Schwann cells. These repair Schwann cells play a multifaceted role in nerve regeneration by clearing myelin debris, secreting regeneration-promoting factors, mediating structural reorganization, and creating a conducive microenvironment for axonal regrowth. Therapeutic strategies targeting the regulation of the EMT-like program of Schwann cells thus hold significant promise for the treatment of peripheral nerve injury, particularly in cases of severe nerve injury with incomplete recovery and poor functional restoration.

Evidence level

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

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