Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy
TLDR
The UUO model is likely to reveal useful biomarkers of progression of renal disease, as well as new therapies, which are desperately needed to allow intervention before the establishment of irreversible renal injury.About:
This article is published in Kidney International.The article was published on 2009-06-01 and is currently open access. It has received 824 citations till now. The article focuses on the topics: Renal fibrosis & Fibrosis.read more
Citations
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Snail1-induced partial epithelial-to-mesenchymal transition drives renal fibrosis in mice and can be targeted to reverse established disease
M. Teresa Grande,Berta Sanchez-Laorden,Cristina López-Blau,Cristina A. de Frutos,Agnès Boutet,Miguel Arévalo,R. Grant Rowe,Stephen J. Weiss,José M. López-Novoa,M. Angela Nieto +9 more
TL;DR: It is shown that the reactivation of Snai1 in mouse renal epithelial cells is required for the development of fibrosis in the kidney and that Snail1-induced fibrosis can be reversed in vivo and that obstructive nephropathy can be therapeutically ameliorated in mice by targeting Snails1 expression.
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Inflammation and EMT: an alliance towards organ fibrosis and cancer progression
TL;DR: The chronic inflammatory microenvironment common to fibrotic and cancer cells emerges as a decisive factor in the induction of the pathological EMT.
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The immune system and kidney disease: basic concepts and clinical implications
TL;DR: The kidneys are frequently targeted by pathogenic immune responses against renal autoantigens or by local manifestations of systemic autoimmunity, causing intestinal barrier dysfunction, systemic inflammation and immunodeficiency that contribute to the morbidity and mortality of patients with kidney disease.
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Inflammatory processes in renal fibrosis.
TL;DR: Understanding the mechanisms by which inflammation drives renal fibrosis is necessary to facilitate the development of therapeutics to halt the progression of chronic kidney disease.
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The NLRP3 Inflammasome Promotes Renal Inflammation and Contributes to CKD
Akosua Vilaysane,Justin Chun,Mark E. Seamone,Wenjie Wang,Rick Chin,Simon A. Hirota,Yan Li,Sharon A. Clark,Jürg Tschopp,Kiril Trpkov,Brenda R. Hemmelgarn,Paul L. Beck,Daniel A. Muruve +12 more
TL;DR: Results strongly support a role for NLRP3 in renal injury and identify the inflammasome as a possible therapeutic target in the treatment of patients with progressive CKD.
References
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Evidence that fibroblasts derive from epithelium during tissue fibrosis
Masayuki Iwano,David Plieth,Theodore M. Danoff,Theodore M. Danoff,Chengsen Xue,Hirokazu Okada,Hirokazu Okada,Eric G. Neilson +7 more
TL;DR: The findings suggest that a substantial number of organ fibroblasts appear through a novel reversal in the direction of epithelial cell fate, which highlights the potential plasticity of differentiated cells in adult tissues under pathologic conditions.
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Hyperfiltration in remnant nephrons : A potentially adverse response to renal ablation
TL;DR: In this article, a study was performed in three groups of male Munich-Wistar rats 1 wk after surgery: group I, eight control rats that underwent laparotomy and were fed a normal diet.
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Identification and characterization of a fibroblast marker: FSP1.
Frank Strutz,Hirokazu Okada,Cecilia W. Lo,Theodore M. Danoff,Robert L. Carone,John E. Tomaszewski,Eric G. Neilson +6 more
TL;DR: Experiments in which the in vitro overexpression of FSP1 cDNA in tubular epithelium is accompanied by conversion to a mesenchymal phenotype are observed, as characterized by a more stellate and elongated fibroblast- like appearance, a reduction in cytokeratin, and new expression of vimentin.
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Fibroblasts in Kidney Fibrosis Emerge via Endothelial-to-Mesenchymal Transition
TL;DR: It is demonstrated that endothelial cells also contribute to the emergence of fibroblasts during kidney fibrosis via the process of endothelial-to-mesenchymal transition (EndMT), and it is suggested that targeting EndMT might have therapeutic potential.
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Pericytes and perivascular fibroblasts are the primary source of collagen-producing cells in obstructive fibrosis of the kidney.
TL;DR: These results serve to refocus fibrosis research to injury of the vasculature rather than injury to the epithelium, and suggest that either vascular injury or vascular factors are the most likely triggers for pericyte migration and differentiation into myofibroblasts.