Abstract

The pathogenesis of systemic sclerosis (SSc; scleroderma) is still enigmatic. Genetic, familial, and twin studies suggest that SSc occurs in genetically susceptible individuals. Recent high-throughput technologies, including gene expression profiling and proteomics, have accelerated the rate of information acquired on possible mechanisms involved in SSc pathogenesis. The potential of the data obtained lies in their use for identifying new disease markers, monitoring disease activity, and developing tailored therapies. The result is an era of unprecedented advance that will benefit SSc and many other diseases.

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