Abstract
Current evidence suggests that fibroblasts undergo phenotypic modulation during several physiologic and pathologic conditions, such as wound healing and fibrocontractive diseases [29]. These phenotypically altered fibroblasts develop cytoskeletal features similar to those of smooth muscle cells (SMCs), including the expression of α-smooth muscle actin (α-SMA), which is a contractile isoform of actin and, hence, they have been denoted as myofibroblasts [8]. The myofibroblast is thought to contribute to the process of wound contraction, as well as contractile phenomena observed during fibrotic diseases. However, little is known about the mechanisms responsible for phenotypic modulation of fibroblasts and the expression of α-SMA. Several types of growth factors and cytokines that are locally released from inflammatory and stromal cells at wound sites, as well as components of the extracellular matrix, have been studied to evaluate their role in fibroblastic differentiation. A likely candidate for regulation of α-SMA is transforming growth factor-β (TGF-β) [7], a potent regulator of matrix remodeling. This regulation may be achieved in part by modulation of cell-matrix interactions.
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Narani, N. et al. (1999). Transforming Growth Factor-β Induction of α-Smooth Muscle Actin Is Dependent on the Deformability of the Collagen Matrix. In: Desmoulière, A., Tuchweber, B. (eds) Tissue Repair and Fibrosis. Current Topics in Pathology, vol 93. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58456-5_6
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DOI: https://doi.org/10.1007/978-3-642-58456-5_6
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