Epithelial Origin of Myofibroblasts during Fibrosis in the Lung

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Abstract
An understanding of the mechanisms underlying pulmonary fibrosis remains elusive. Once believed to result primarily from chronic inflammation, it is now clear that inflammation and chronic fibrosis, especially in diseases such as idiopathic pulmonary fibrosis/usual interstitial pneumonia, are often dissociated, and that inflammation is neither necessary nor sufficient to induce fibrosis. The origin of the primary effector cell of fibrosis in the lung, the myofibroblast, is not clearly established. Three potential sources have been hypothesized. Although conversion of resident fibroblasts and differentiation of circulating bone marrow–derived progenitors likely play a role, the possible contribution of alveolar epithelial cells (AECs), through a process termed “epithelial–mesenchymal transition” (EMT), has only recently received consideration. A process by which epithelial cells lose cell–cell attachment, polarity and epithelial-specific markers, undergo cytoskeletal remodeling, and gain a mesenchymal phen...

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