Abstract
Systemic sclerosis (SSc) is a connective tissue disorder representing fibrosis in the skin and internal organs such as lungs. An activated differentiation of local progenitor cells to myofibroblasts is likely a key mechanism underlying overproduction of extracellular matrix and resultant tissue fibrosis in SSc. Calpains are family members of Ca2+-dependent cysteine proteases for which the biological action may contribute to fibrosis in various organs. However, the precise mechanism of calpain-dependent fibrosis and therapeutic utility of their inhibitors in SSc remain unclear.
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