Tissue Repair, Contraction and the Myofibroblast

Summarizes the findings concerning the biology of the myofibroblast, a cell involved in the evolution and contraction of granulation tissue and of fibrotic changes. This title shows that the myofibroblast is responsible for the development of hypertrophic scars, pulmonary and renal fibrosis and bronchial asthma.

---

hirty-four years after the first description of the myofibroblast, the number of publications concerning this cell is very impressive and Tcontinuously expanding, and the work on the myofibroblast involves many laboratories throughout the world. The myofibroblast has been implicated in developmental and physiological phenomena, as well as in a variety of pathological situations, going from wound healing and fibrotic changes to asthma and cancer invasion. Many aspects of myofibroblast biology have been clarified, such as the role of TGF-P and ED-A cellular fibronectin in its differentiation and the role of a-smooth muscle actin in tension production by this cell; however several important problems concerning myofibroblast origin, ftmction and participation in pathological processes remain to be solved. The purpose of this book, as well of the Meeting "Tissue Repair, Contraction and the Myofibroblast" that took place in Nyon, near Geneva, Switzerland on November 18-20, 2004, is to put together the most recent advances in the understanding of myofibroblast biology and to present the main directions of research taking place worldwide to explore new aspects of myofibroblast physiological and pathological activities, such as: mechanisms of force generation by the myofibroblast; myofibroblast origin and diversity; interaction of the myofibroblast with other cells, normal and malignant epithelial cells in particular; and participation of the myofibroblast in the development of fibrosis in various organs. If we consider the animated and constructive discussions that took place during the Nyon Meeting, we are sure that this book will inspire new research in these fields.