Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 179, Issue 3, Pages 1074-1080Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2011.06.001
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- National Institutes of Health [5 R01 AR19616]
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The accumulation of a large number of myofibroblasts is responsible for exaggerated and uncontrolled production of extracellular matrix during the development and progression of pathological fibrosis. Myofibroblasts in fibrotic tissues are derived from at least three sources: expansion and activation of resident tissue fibroblasts, transition of epithelial cells into mesenchymal cells (epithelial-mesenchymal transition, EMT), and tissue migration of bone marrow-derived circulating fibrocytes. Recently, endothelial to mesenchymal transition (EndoMT), a newly recognized type of cellular transdifferentiation, has emerged as another possible source of tissue myofibroblasts. EndoMT is a complex biological process in which endothelial cells lose their specific markers and acquire a mesenchymal or myofibroblastic phenotype and express mesenchymal cell products such as a smooth muscle actin (alpha-SMA) and type I collagen. Similar to EMT, EndoMT can be induced by transforming growth factor (TGF-beta). Recent studies using cell-lineage analysis have demonstrated that EndoMT may be an important mechanism in the pathogenesis of pulmonary, cardiac, and kidney fibrosis, and may represent a novel therapeutic target for fibrotic disorders. (Am J Pathol 2011, 179:1074-1080; DOI: 10.1016/j.ajpath.2011.06.001)
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