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https://www.readbyqxmd.com/read/22949934/telmisartan-counteracts-tgf-%C3%AE-1-induced-epithelial-to-mesenchymal-transition-via-ppar-%C3%AE-in-human-proximal-tubule-epithelial-cells
#1
Yumin Chen, Qiong Luo, Zibo Xiong, Wei Liang, Li Chen, Zuying Xiong
Chronic renal failure (CRF) mainly results from kidney fibrosis. Epithelial-to-mesenchymal transition (EMT) occurs in stressed tubular epithelial cells and contributes to renal fibrosis. Transforming growth factor-β1 (TGF-β1) has been shown to initiate and complete the whole EMT process. Peroxisome proliferators-activated receptor-γ (PPAR-γ) exerts anti-inflammatory, anti-fibrotic and vaculo-protective effects on different renal diseases. Telmisartan is a member of angiotensin II (Ang II) receptor blocker (ARB) family...
2012: International Journal of Clinical and Experimental Pathology
https://www.readbyqxmd.com/read/22326534/candesartan-antagonizes-pressure-overload-evoked-cardiac-remodeling-through-smad7-gene-dependent-mmp-9-suppression
#2
Hong Yu, Gang Zhao, Hui Li, Xiaojian Liu, Shijun Wang
The present study was designed to investigate the underlying molecular mechanism for Angiotensin II type 1 receptor blockers (ARBs) mediated cardio-protection against pressure overload-induced cardiac remodeling with a focus on Smad7. ROCK-1, Smad3 and fibronectin expressions were increased in male C57BL/6 mice underwent transverse aortic constriction (TAC) for 2weeks. Treatment with Candesartan (2mg/kg per day) could effectively downregulate Smad3 and fibronectin accompanied by upregulating of Smad7. Further data showed that Candesartan inhibited TGF-β1 signal-induced epithelial-to-mesenchymal transition (EMT) through attenuating matrix metalloproteinases (MMP-9), such effect was abolished by knocking-down Smad7...
April 15, 2012: Gene
https://www.readbyqxmd.com/read/22043587/an-update-on-raas-blockade-and-peritoneal-membrane-preservation-the-ace-of-art
#3
REVIEW
Wassawon Wontanatawatot, Somchai Eiam-Ong, Asada Leelahavanichkul, Talerngsak Kanjanabuch
Peritoneal membrane changes over time in long-term peritoneal dialysis (PD) patients lead to dialysis failure and increased morbidity as well as mortality. Bio-incompatable PD solution, peritonitis, and uremia are hypothesized in causing membrane damage. Fibrous organization and angiogenesis of peritoneum are crucial morphological alterations which can diminish the efficacy of exchange and cause ultrafiltration failure. Pathophysiologic mechanisms of membrane damage have been extensively studied to innovate therapeutic strategies...
September 2011: Journal of the Medical Association of Thailand, Chotmaihet Thangphaet
https://www.readbyqxmd.com/read/20848133/differential-susceptibility-to-epithelial-mesenchymal-transition-emt-of-alveolar-bronchial-and-intestinal-epithelial-cells-in-vitro-and-the-effect-of-angiotensin-ii-receptor-inhibition
#4
Stephen T Buckley, Carlos Medina, Carsten Ehrhardt
The generation of myofibroblasts via epithelial-mesenchymal transition (EMT), a process through which epithelial cells lose their polarity and become motile mesenchymal cells, is a proposed contributory factor in fibrosis of a number of organs. Currently, it remains unclear to what extent epithelia of the upper airways and large intestine are susceptible to this process. Herein, we investigated the ability of model cell lines of alveolar (A549), bronchial (Calu-3) and colonic (Caco-2) epithelial cells to undergo EMT when challenged with transforming growth factor-β1 (TGF-β1) and other pro-inflammatory cytokines...
October 2010: Cell and Tissue Research
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