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10.18632/oncotarget.9058 http://scihub22266oqcxt.onion/10.18632/oncotarget.9058 C5095017!5095017!27145370     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2016 ; 7 (24): 36510-28 Nephropedia Template TP {{tp|p=27145370|t=2016. CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPAR? pathway |pdf=|usr=}}{{27145370}} gab.com Text CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPAR pathway JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27145370 #FOAvip Cyclin-dependent kinase 5 (CDK5) has been documented in podocyte injuries in diabetic nephropathy (DN), however its role in renal tubular epithelial cells has not been elucidated. We report here that CDK5 is detrimental and promotes tubulointerstitial fibrosis (TIF) via the extracellular signal-regulated kinase 1/2 (ERK1/2)/peroxisome proliferator-activated receptor gamma (PPRA?) pathway in DN. In high glucose cultured NRK52E cells, blocking CDK5 activity inhibited epithelial-to-mesenchymal transition (EMT) and fibrosis via ERK1/2/PPAR? pathway. In diabetic rats, CDK5 inhibitor roscovitine decreased renal fibrosis and improved renal function as demonstrated by a decrease in levels of blood urine nitrogen (BUN), serum creatinine and ?2-microglobulin. Further studies revealed that improved renal fibrosis and function in diabetic rats were associated with inactivation of ERK1/2 and PPAR? signaling pathways. In late staged DN patients, the upregulation of CDK5 and p35 activated phosphorylated ERK1/2 and PPAR?, leading to decreased levels of E-cadherin but increased Vimentin and Collagen IV. Accordingly, renal fibrosis and function were worsened as revealed by decreased estimated glomerular filtration rate (eGFR) and increased serum BUN, creatinine, ?2-microglobulin, 24-hour proteinuria and urine albumin to creatinine ratio (UACR). These findings demonstrate a novel mechanism that CDK5 increases tubulointerstitial fibrosis by activating the ERK1/2/PPAR? pathway and EMT in DN. CDK5 might have therapeutic potential in diabetic nephropathy. Twit Text FOAVip CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPAR pathway ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27145370 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27145370 #FOAvip English Wikipedia <ref>{{Cite pmid|27145370}}</ref> CDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropathy via ERK1/2/PPAR? pathway #MMPMID27145370 Bai X; Hou X; Tian J; Geng J; Li X Oncotarget 2016[Jun]; 7 (24): 36510-28 PMID27145370show ga Cyclin-dependent kinase 5 (CDK5) has been documented in podocyte injuries in diabetic nephropathy (DN), however its role in renal tubular epithelial cells has not been elucidated. We report here that CDK5 is detrimental and promotes tubulointerstitial fibrosis (TIF) via the extracellular signal-regulated kinase 1/2 (ERK1/2)/peroxisome proliferator-activated receptor gamma (PPRA?) pathway in DN. In high glucose cultured NRK52E cells, blocking CDK5 activity inhibited epithelial-to-mesenchymal transition (EMT) and fibrosis via ERK1/2/PPAR? pathway. In diabetic rats, CDK5 inhibitor roscovitine decreased renal fibrosis and improved renal function as demonstrated by a decrease in levels of blood urine nitrogen (BUN), serum creatinine and ?2-microglobulin. Further studies revealed that improved renal fibrosis and function in diabetic rats were associated with inactivation of ERK1/2 and PPAR? signaling pathways. In late staged DN patients, the upregulation of CDK5 and p35 activated phosphorylated ERK1/2 and PPAR?, leading to decreased levels of E-cadherin but increased Vimentin and Collagen IV. Accordingly, renal fibrosis and function were worsened as revealed by decreased estimated glomerular filtration rate (eGFR) and increased serum BUN, creatinine, ?2-microglobulin, 24-hour proteinuria and urine albumin to creatinine ratio (UACR). These findings demonstrate a novel mechanism that CDK5 increases tubulointerstitial fibrosis by activating the ERK1/2/PPAR? pathway and EMT in DN. CDK5 might have therapeutic potential in diabetic nephropathy. äCDK5 promotes renal tubulointerstitial fibrosis in diabetic nephropath(epmc).pdf DeepDyve Pubget Overpricing