Epithelial to mesenchymal transition in renal fibrogenesis: pathologic significance, molecular mechanism, and therapeutic intervention.

By Youhua Liu. Journal of the American Society of Nephrology, 2004

1,130 citations recorded by the source corpus.

Subfields: Molecular Biology, Nephrology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/cd3c94c06386e3fb59f4f65645f8342ccafa813d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Nephrology

In Pulmonary and Respiratory Medicine

Citations in the corpus

Cellular and molecular mechanisms of renal fibrosis (2011, background): “The frequency at which epithelial cells complete the entire EMT course and ultimately become fibroblasts is probably limited, and depends heavily on the disease models, stages and persistence of raised cytokine pressure in the inflamed milieu”
Fate tracing reveals the pericyte and not epithelial origin of myofibroblasts in kidney fibrosis. (2010, background): “Explanations for a failure to make these observations in fixed tissues include the hypothesis that a cell exiting the confines of the basement membrane rapidly loses epithelial markers and only subsequently gains myofibroblast markers.(35) However, in vitro, epithelial cells can express both fibrobl”
Fibroblasts in fibrosis: novel roles and mediators (2014, background): “The EMT has been observed as a source of myofibroblasts in kidney fibrosis (Ng et al., 1998; Jinde et al., 2001; Liu, 2004); however, subsequent attempts to trace such phenomena in the skin, lung, heart, and liver have been largely unsuccessful in vivo, suggesting that EMT-mediated formation of…”
Renal tubule injury: a driving force toward chronic kidney disease. (2018, background): “TECs might contribute directly to renal fibrosis via epithelialmesenchymal transition (EMT), a phenotypic conversion program that is characterized by the loss of epithelial markers (such as E-cadherin, zonula occludens-1, and cytokeratin) and by the gain of mesenchymal features (including vimentin, ”
TGF-β-induced EMT: mechanisms and implications for fibrotic lung disease (2007, background): “3 to a mesenchymal phenotype giving rise to fibroblasts and myofibroblasts, is increasingly recognized as playing an integral role in the process of repair and scar formation following epithelial injury in a number of tissues (35, 55).”
EMT and tumor metastasis (2015, background): “4% TGF-β, BMP-7, Claudin-1, HDAC1,2,3, hepatocyte growth factor, Klf8, miR-23b, miR-29b, miR-34, miRs-141/200, miR-205, miR-438-3p, [62,66,72-74]”
TGF-β1 induces human alveolar epithelial to mesenchymal cell transition (EMT) (2005, background): “Thus, one possible role of TGF-β1 in IPF is to induce or promote epithelial cells in injured alveolar epithelium to undergo EMT [15], as is evident from studies of other fibrotic disorders such as renal fibrosis [10,11,14].”
Epithelial cell cycle arrest in G2/M mediates kidney fibrosis after injury (2010, neutral): “Whereas tubular epithelial cells have been proposed to have an active role in the progression of fibrosis via epithelial-to-mesenchymal transformatio”
Complex networks orchestrate epithelial–mesenchymal transitions (2006, background): “Fibrosis is characterized by increased numbers of myofibroblasts that deposit interstitial ECM, and a significant fraction of these fibroblasts are thought to arise through EMT of the tubular epithelial cell”
Carcinoma invasion and metastasis: a role for epithelial-mesenchymal transition? (2005, background): “Pathologically, fibroblast cells are produced by an EMTlikemechanism in fibrotic kidney, and these cells remain local (18, 19).”