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

Cutaneous fibrosis takes place due to chronic inflammation, tissue trauma, or autoimmune reactions. It is marked by abnormal tissue remodeling; such remodeling is characterized by a raised quantity of myofibroblasts and an excessive accumulation of extracellular matrix (ECM) in the dermis. Therefore, this abnormal process brings about a decrease in tissue function, causes structural irregularities, and thus severely lowers patients' quality of life. Although remarkable progressions have been achieved in preventive and treatment methods, the molecular processes under cutaneous fibrosis are not fully comprehended. Epithelial-mesenchymal transition (EMT) is a dynamic and strictly controlled biological phenomenon where epithelial cells discard their epithelial characteristics and obtain mesenchymal properties. Hence, newly appearing data has demonstrated that EMT plays a critical role in the development of fibrotic disorders. EMT has been proposed as a potential contributor to fibrogenesis, although its quantitative contribution and pathological significance relative to resident fibroblasts and other mesenchymal cell sources remain to be further clarified. These findings not only increase our knowledge of the pathophysiology of cutaneous fibrosis but also identify new molecular targets that can be utilized for therapeutic aims. This review collects the latest progressions in understanding the role of EMT in cutaneous fibrotic disorders. The objective is to provide new understandings into the regulatory mechanisms and possible treatment ways for this condition.