Myofibroblasts: Biochemical and Proteomic Approaches to Fibrosis

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  • Honda Eiko
    Life Science Research Institute, Kinki University
  • Park Ah-Mee
    Department of Biochemistry, Kinki University Faculty of Medicine
  • Yoshida Koji
    Department of Biochemistry, Kinki University Faculty of Medicine
  • Tabuchi Masaki
    Department of Biochemistry, Kinki University Faculty of Medicine
  • Munakata Hiroshi
    Department of Biochemistry, Kinki University Faculty of Medicine

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Fibrosis is a state, in which excess amounts of extracellular matrix are deposited in the tissue. Fibrosis can occur in various organs, including the liver, lung, kidney and heart. The progression of fibrosis involves interstitial hypercellularity, accumulation of extracellular matrix, and atrophy of epithelial structures, resulting in a loss of normal function. Myofibroblasts play a crucial role in the development and progress of fibrosis. When stimulated, myofibroblasts actively synthesize connective tissue components and cause organ fibrosis. As a result, the process and the mechanism of myofibroblast activation represent a target for antifibrotic treatment. As yet, however, an effective treatment has not been developed, and new treatment modalities are expected. Because activation of myofibroblasts is a key event during fibrosis development, there is great interest in identifying and characterizing proteins whose expression is changed after this activation. In this review, fibrosis is outlined and the role of myofibroblasts in this disorder is described. Furthermore, the search for candidate proteins to target for treatment and the prospects of antifibrotic therapy are discussed.

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