MATRIX METALLOPROTEINASES AND THEIR INHIBITORS IN PATIENTS WITH SCLERODERMA.

Abstract

Scleroderma (SD) holds a significant place in modern dermatology, ranking second in prevalence among dermatological conditions. However, its exact pathogenesis remains insufficiently understood. One proposed primary mechanism for the development of sclerotic changes in the skin involves the activation of fibrogenesis, which is thought to stem from dysfunction within the extracellular matrix (ECM). The ECM is composed of structural proteins such as collagen, elastin, proteoglycans, and glycoproteins, all of which are regulated by a specific class of proteolytic enzymes called matrix metalloproteinases (MMPs). These enzymes are critical for maintaining ECM homeostasis and influence key biological molecules, including cytokines, interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), transforming growth factor β1 (TGF-β1), and vascular endothelial growth factor (VEGF)