2013
DOI: 10.1097/bor.0b013e32835b1352
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Myofibroblasts

Abstract: Purpose of review Interest in the myofibroblast as a key player in propagation of chronic progressive fibrosis continues to elicit many publications, with focus on its cellular origins and the mechanisms underpinning their differentiation and/or transition. The objective of the review is to highlight this recent progress. Recent findings The epithelial origin of the myofibroblast in fibrosis has been challenged by recent studies, with the pericyte suggested as a possible precursor instead. Additional signali… Show more

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Cited by 96 publications
(76 citation statements)
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References 94 publications
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“…The expression of a-smooth muscle actin (a-SMA) is a widely recognized marker for this transition but it also contributes to the maintenance of fibrosis (Sappino et al, 1990;Boukhalfa et al, 1996;Zhang et al, 1996;Tomasek et al, 2002;Gilbane et al, 2013;Hu and Phan, 2013). There are multiple signaling pathways that induce myofibroblast transition.…”
Section: Introductionmentioning
confidence: 99%
See 1 more Smart Citation
“…The expression of a-smooth muscle actin (a-SMA) is a widely recognized marker for this transition but it also contributes to the maintenance of fibrosis (Sappino et al, 1990;Boukhalfa et al, 1996;Zhang et al, 1996;Tomasek et al, 2002;Gilbane et al, 2013;Hu and Phan, 2013). There are multiple signaling pathways that induce myofibroblast transition.…”
Section: Introductionmentioning
confidence: 99%
“…A central feature of virtually all diseases of fibrosis is the activation of fibroblasts and their transition into myofibroblasts (Sappino et al, 1990;Boukhalfa et al, 1996;Zhang et al, 1996;Beyer et al, 2010;Hinz et al, 2012;Wynn and Ramalingam, 2012;Gilbane et al, 2013;Hu and Phan, 2013). The expression of a-smooth muscle actin (a-SMA) is a widely recognized marker for this transition but it also contributes to the maintenance of fibrosis (Sappino et al, 1990;Boukhalfa et al, 1996;Zhang et al, 1996;Tomasek et al, 2002;Gilbane et al, 2013;Hu and Phan, 2013).…”
Section: Introductionmentioning
confidence: 99%
“…Therefore, FIZZ1 could cause dedifferentiation of adipocytes followed by differentiation into myofibroblasts in vitro, consistent with a role in adipocyte transdifferentiation to the myofibroblast, a key cell in pathogenesis of chronic fibrosis. 4,29 However, because FIZZ1 caused incomplete (<60%) inhibition of adipocyte gene marker expression, direct adipocyte-to-myofibroblast transdifferentiation without going through a dedifferentiated state cannot be ruled out.…”
Section: Adipocyte Dedifferentiation and Myofibroblast Differentiationmentioning
confidence: 99%
“…3 Moreover, suppression of adipogenesis results in marked reduction in myofibroblast numbers in the wound bed, suggesting that adipocytes may also be important in chronic fibrotic disorders wherein myofibroblasts are known to play a key role. 4 However, other studies suggest that inhibition of adipocyte differentiation by profibrotic factors such as transforming growth factor (TGF)-b1 is associated with dermal fibrosis in an animal model. 5 The mechanism may be mediated by TGF-b1 suppression of peroxisome proliferator-activated receptor (PPAR)-g expression a key indicator of adipocyte differentiation.…”
mentioning
confidence: 99%
“…During EndoMT, endothelial cells (EC) lose their molecular markers such as VE-cadherin, detach from endothelial layer and begin the expression of mesenchymal cell products (e.g. α-SMA) (20).…”
Section: Endothelial Mesenchymal Transition (Endomt)mentioning
confidence: 99%