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Published online before print April 19, 2007
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Biological Perspectives |
From the Laboratory of Cell Biophysics,* École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; the Department of Pathology, University of Michigan Medical School, Ann Arbor, Michigan; the Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, Michigan; the Department of Clinical Pathophysiology, University of Florence, Florence, Italy; and the Department of Immunology and Pathology,¶ C.M.U., University of Geneva, Geneva, Switzerland
Abstract
The crucial role played by the myofibroblast in wound healing and pathological organ remodeling is well established; the general mechanisms of extracellular matrix synthesis and of tension production by this cell have been amply clarified. This review discusses the pattern of myofibroblast accumulation and fibrosis evolution during lung and liver fibrosis as well as during atheromatous plaque formation. Special attention is paid to the specific features characterizing each of these processes, including the spectrum of different myofibroblast precursors and the distinct pathways involved in the formation of differentiated myofibroblasts in each lesion. Thus, whereas in lung fibrosis it seems that most myofibroblasts derive from resident fibroblasts, hepatic stellate cells are the main contributor for liver fibrosis and media smooth muscle cells are the main contributor for the atheromatous plaque. A better knowledge of the molecular mechanisms conducing to the appearance of differentiated myofibroblasts in each pathological situation will be useful for the understanding of fibrosis development in different organs and for the planning of strategies aiming at their prevention and therapy.
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