Abstract
Scleroderma (systemic sclerosis) is characterized by the deposition and accumulation of excessive amounts of collagen and extracellular-matrix molecules, the dysfunction of microvascular endothelial cells, and altered immune tolerance. These interacting and interdependent processes lead to chronic inflammation and tissue fibrosis.To investigate complex mechanisms of disease pathogenesis, conventional wisdom dictates that a single aspect of disease be dissected out and examined in detail. The skin is a prominent target organ in scleroderma, and fibroblasts from affected patients are activated and display a variety of properties, including increased production of collagens and other extracellular-matrix proteins, abnormal growth patterns, and resistance to . . .
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