Epithelial–mesenchymal transition in cutaneous fibrosis disease: from mechanisms to therapy

To provide insights into the regulatory mechanisms and treatment options for cutaneous fibrosis, focusing on epithelial–mesenchymal transition (EMT).

Cutaneous fibrosis results from chronic inflammation, tissue trauma, or autoimmune reactions, leading to abnormal ECM accumulation.
EMT plays a critical role in the development of fibrotic disorders, potentially serving as a source of myofibroblasts.
Three subtypes of EMT are identified: Type I (embryogenesis), Type II (tissue repair), and Type III (cancer progression).
Basal keratinocytes can undergo EMT under fibrotic conditions, contributing to dermal fibrogenesis.

The findings enhance understanding of the pathophysiology of cutaneous fibrosis.

The quantitative contribution of EMT relative to resident fibroblasts in fibrogenesis remains unclear.
Current therapeutic strategies for cutaneous fibrosis are largely inadequate.

The review suggests that targeting EMT may be a potential therapeutic approach for treating cutaneous fibrosis.