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10.1038/mt.2013.235 http://scihub22266oqcxt.onion/10.1038/mt.2013.235 C3982502!3982502!24445937     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24445937&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Ther 2014 ; 22 (4): 842-53 Nephropedia Template TP {{tp|p=24445937|t=2014. MicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice |pdf=|usr=}}{{24445937}} gab.com Text MicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice JO: Mol Ther http://www.kidney.de/pget.php?&tw=1&pmid=24445937 #FOAvip Inflammation and its consequent fibrosis are two main features of diabetic nephropathy (DN), but target therapy on these processes for DN remains yet ineffective. We report here that miR-29b is a novel therapeutic agent capable of inhibiting progressive renal inflammation and fibrosis in type 2 diabetes in db/db mice. Under diabetic conditions, miR-29b was largely downregulated in response to advanced glycation end (AGE) product, which was associated with upregulation of collagen matrix in mesangial cells via the transforming growth factor-? (TGF-?)/Smad3-dependent mechanism. These pathological changes were reversed by overexpressing miR-29b, but enhanced by knocking-down miR-29b. Similarly, loss of renal miR-29b was associated with progressive diabetic kidney injury, including microalbuminuria, renal fibrosis, and inflammation. Restored renal miR-29b by the ultrasound-based gene therapy was capable of attenuating diabetic kidney disease. Further studies revealed that inhibition of Sp1 expression, TGF-?/Smad3-dependent renal fibrosis, NF-?B?driven renal inflammation, and T-bet/Th1-mediated immune response may be mechanisms associated with miR-29b treatment in db/db mice. In conclusion, miR-29b may play a protective role in diabetic kidney disease and may have therapeutic potential for diabetic kidney complication. Twit Text FOAVip MicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice ????Mol Ther http://www.kidney.de/pget.php?&tw=1&pmid=24445937 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24445937 #FOAvip English Wikipedia <ref>{{Cite pmid|24445937}}</ref> MicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice #MMPMID24445937 Chen HY; Zhong X; Huang XR; Meng XM; You Y; Chung AC; Lan HY Mol Ther 2014[Apr]; 22 (4): 842-53 PMID24445937show ga Inflammation and its consequent fibrosis are two main features of diabetic nephropathy (DN), but target therapy on these processes for DN remains yet ineffective. We report here that miR-29b is a novel therapeutic agent capable of inhibiting progressive renal inflammation and fibrosis in type 2 diabetes in db/db mice. Under diabetic conditions, miR-29b was largely downregulated in response to advanced glycation end (AGE) product, which was associated with upregulation of collagen matrix in mesangial cells via the transforming growth factor-? (TGF-?)/Smad3-dependent mechanism. These pathological changes were reversed by overexpressing miR-29b, but enhanced by knocking-down miR-29b. Similarly, loss of renal miR-29b was associated with progressive diabetic kidney injury, including microalbuminuria, renal fibrosis, and inflammation. Restored renal miR-29b by the ultrasound-based gene therapy was capable of attenuating diabetic kidney disease. Further studies revealed that inhibition of Sp1 expression, TGF-?/Smad3-dependent renal fibrosis, NF-?B?driven renal inflammation, and T-bet/Th1-mediated immune response may be mechanisms associated with miR-29b treatment in db/db mice. In conclusion, miR-29b may play a protective role in diabetic kidney disease and may have therapeutic potential for diabetic kidney complication. äMicroRNA-29b Inhibits Diabetic Nephropathy in db/db Mice (epmc).pdf DeepDyve Pubget Overpricing