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Cutaneous fibrosis is the accumulation of extracellular matrix (ECM) components in the dermis, leading to compromised function and altered architecture of the dermis. Development of fibrosis occurs naturally during scar formation in wound repair or is a pathological process in pro-fibrotic diseases. Cutaneous fibrosis is a fundamental feature of fatty skin sclerosis and is associated with increased levels of the cytokine transforming growth factor-β,186. This growth factor may be derived from activated leukocytes, recruit’s macrophages and fibroblasts into the tissue and leads to the production of extracellular matrix proteins by dermal fibroblasts. The goal of skin fibrosis treatment is the restore abnormally activated dermal fibroblasts producing the excessive amount of extracellular matrix, which is generally a final consequence of the complex disease process including the activation of vascular and immune systems. The prototype of fibrotic skin disease is scleroderma, which can be divided into whole body and local forms. Progressive systemic sclerosis (PSS) is a widespread connective tissue disease in which the fibrotic process affects not only the skin but also the lungs, heart, kidneys and gastrointestinal tract.
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