Fibroblasts in kidney fibrosis emerge via endothelial-to-mesenchymal transition.

By E. Zeisberg, S. Potenta, H. Sugimoto, M. Zeisberg, Raghu Kalluri. Journal of the American Society of Nephrology, 2008

894 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/3a54aa60df4057d56813f9daf70cf234e73980bf

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Citations in the corpus

TGF-β/Smad signaling in renal fibrosis (2015, background): “…signaling with inhibitors or antagonists attenuates or reverses the process of EMT or EndMT (Fan et al., Frontiers in Physiology | www.frontiersin.org 3 March 2015 | Volume 6 | Article 82 1999; Zeisberg et al., 2003, 2008; Li et al., 2010; Liu, 2010; Yang et al., 2010; Xavier et al., 2014).”
Epithelial-mesenchymal transitions in development and disease. (2009, background): “EMT involving transformation of endothelial cells into mesenchymal cells is evident during cardiac and renal fibrosis (EndMT) (Zeisberg et al., 2007a, 2008).”
The metastatic niche: adapting the foreign soil (2009, background): “Intriguingly, in the setting of non-malignant kidney fibrosis, it has been reported that activated fibroblasts not only arise through epithelial–mesenchymal transition (EMT) and recruitment from the bone marrow, but also may emerge through endothelial–mesenchymal transitio”
Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy. (2009, background): “This problem can be addressed with the application of molecular lineage tracing techniques.(33,35) The use of immunohistochemistry to localize individual cell types can be combined with digital morphometry to quantitate the parameters and to make statistical comparisons.”
Cellular and molecular mechanisms of renal fibrosis (2011, background): “Similarly, fibroblasts and/or myofibroblasts might derive from capillary endothelium by endothelial–mesenchymal transition (EndoMT)”
Cellular and molecular mechanisms in kidney fibrosis. (2014, positive): “Using the Six2 Similarly, there have been attempts to map endothelial cell fate, which is a very difficult task since recent insights indicate endothelial-specific markers lack specificity for endothelium (11, 55).”
Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. (2010, background): “Further, a recent report suggests that other terminally differentiated cells such as endothelial cells can develop a myofibroblast phenotype in vitro and in vivo.(11,12) It has been postulated that during kidney injury in vivo, epithelial cells undergo a phenotypic transition or can transdifferentia”
Inflammation and EMT: an alliance towards organ fibrosis and cancer progression (2009, background): “…above, TGF-b1 contributes to the formation of myofibroblasts through the activation of resident fibroblasts and by inducing the transition to mesenchyme of epithelial and endothelial cells via EMT or EndMT, respectively (Zavadil & Böttinger, 2005; Zeisberg & Kalluri, 2008; Zeisberg et al, 2008).”