
The hallmark of scleroderma is fibrosis by excessive extracellular matrix (ECM) deposition in the skin, lung, and other organs. Increasing evidence suggests that overexpression of transforming growth factor-beta (TGF-beta) and its receptors play a key pathogenic role in the development of tissue fibrosis in scleroderma. TGF-beta is known to induce the expression of ECM proteins in the pathogenesis of fibrosis in systemic sclerosis. Investigations into TGF-beta pathways will suggest new treatment strategies for fibrotic diseases.
Extracellular Matrix Proteins, Scleroderma, Systemic, Transforming Growth Factor beta, Animals, Humans, Fibroblasts, Fibrosis, Receptors, Transforming Growth Factor beta, Extracellular Matrix
Extracellular Matrix Proteins, Scleroderma, Systemic, Transforming Growth Factor beta, Animals, Humans, Fibroblasts, Fibrosis, Receptors, Transforming Growth Factor beta, Extracellular Matrix
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