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10.1681/ASN.2011010046 http://scihub22266oqcxt.onion/10.1681/ASN.2011010046 22052053!3269918!22052053     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2012 ; 23 (1): 37-48 Nephropedia Template TP {{tp|p=22052053|t=2012. Antifibrotic effect of tamoxifen in a model of progressive renal disease |pdf=|usr=}}{{22052053}} gab.com Text Antifibrotic effect of tamoxifen in a model of progressive renal disease JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=22052053 #FOAvip Tamoxifen, a selective estrogen receptor modulator, has antifibrotic properties; however, whether it can attenuate renal fibrosis is unknown. In this study, we tested the effects of tamoxifen in a model of hypertensive nephrosclerosis (chronic inhibition of nitric oxide synthesis with L-NAME). After 30 days, treated rats had significantly lower levels of albuminuria as well as lower histologic scores for glomerulosclerosis and interstitial fibrosis than untreated controls. Tamoxifen was renoprotective despite having no effect on the sustained, severe hypertension induced by L-NAME. Tamoxifen prevented the accumulation of extracellular matrix by decreasing the expression of collagen I, collagen III, and fibronectin mRNA and protein. These renoprotective effects associated with inhibition of TGF-beta1 and plasminogen activator inhibitor-1, and with a significant reduction in alpha-smooth muscle actin-positive cells in the renal interstitium. Furthermore, tamoxifen abrogated IL-1beta- and angiotensin-II-induced proliferation of fibroblasts from both kidney explants and from the NRK-49F cell line. Tamoxifen also inhibited the expression of extracellular matrix components and the production and release of TGF-beta1 into the supernatant of these cells. In summary, tamoxifen exhibits antifibrotic effects in the L-NAME model of hypertensive nephrosclerosis, likely through the inhibition of TGF-beta1, suggesting that it may have therapeutic use in CKD treatment. Twit Text FOAVip Antifibrotic effect of tamoxifen in a model of progressive renal disease ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=22052053 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=22052053 #FOAvip English Wikipedia <ref>{{Cite pmid|22052053}}</ref> Antifibrotic effect of tamoxifen in a model of progressive renal disease #MMPMID22052053 Delle H; Rocha JR; Cavaglieri RC; Vieira JM Jr; Malheiros DM; Noronha IL J Am Soc Nephrol 2012[Jan]; 23 (1): 37-48 PMID22052053show ga Tamoxifen, a selective estrogen receptor modulator, has antifibrotic properties; however, whether it can attenuate renal fibrosis is unknown. In this study, we tested the effects of tamoxifen in a model of hypertensive nephrosclerosis (chronic inhibition of nitric oxide synthesis with L-NAME). After 30 days, treated rats had significantly lower levels of albuminuria as well as lower histologic scores for glomerulosclerosis and interstitial fibrosis than untreated controls. Tamoxifen was renoprotective despite having no effect on the sustained, severe hypertension induced by L-NAME. Tamoxifen prevented the accumulation of extracellular matrix by decreasing the expression of collagen I, collagen III, and fibronectin mRNA and protein. These renoprotective effects associated with inhibition of TGF-beta1 and plasminogen activator inhibitor-1, and with a significant reduction in alpha-smooth muscle actin-positive cells in the renal interstitium. Furthermore, tamoxifen abrogated IL-1beta- and angiotensin-II-induced proliferation of fibroblasts from both kidney explants and from the NRK-49F cell line. Tamoxifen also inhibited the expression of extracellular matrix components and the production and release of TGF-beta1 into the supernatant of these cells. In summary, tamoxifen exhibits antifibrotic effects in the L-NAME model of hypertensive nephrosclerosis, likely through the inhibition of TGF-beta1, suggesting that it may have therapeutic use in CKD treatment. |Animals[MESH] |Antineoplastic Agents, Hormonal/*therapeutic use[MESH] |Cell Proliferation/drug effects[MESH] |Cells, Cultured[MESH] |Down-Regulation/drug effects[MESH] |Drug Evaluation, Preclinical[MESH] |Extracellular Matrix/drug effects[MESH] |Fibroblasts/*drug effects/metabolism[MESH] |Fibrosis[MESH] |Kidney Diseases/*drug therapy/pathology[MESH] |Kidney/metabolism/pathology[MESH] |Male[MESH] |Plasminogen Activator Inhibitor 1/metabolism[MESH] |Rats[MESH] |Rats, Wistar[MESH] |Tamoxifen/pharmacology/*therapeutic use[MESH]Antifibrotic effect of tamoxifen in a model of progressive renal disea(epmc).pdf DeepDyve Pubget Overpricing