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)
