Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1186/s12902-017-0200-8 http://scihub22266oqcxt.onion/10.1186/s12902-017-0200-8 28774305!5543752!28774305     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28774305&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       BMC+Endocr+Disord 2017 ; 17 (1): 48 Nephropedia Template TP {{tp|p=28774305|t=2017. Renal injury is accelerated by global hypoxia-inducible factor 1 alpha deficiency in a mouse model of STZ-induced diabetes |pdf=|usr=}}{{28774305}} gab.com Text Renal injury is accelerated by global hypoxia-inducible factor 1 alpha deficiency in a mouse model of STZ-induced diabetes JO: BMC Endocr Disord http://www.kidney.de/pget.php?&tw=1&pmid=28774305 #FOAvip BACKGROUND: Hypoxia inducible factor 1 (HIF-1) activates protective pathways to counteract hypoxia and prevent tissue damage in conjunction with renal injury. The aim of this study was to evaluate a role of HIF-1 in diabetes-induced kidney damage. METHODS: We used a streptozotocin-induced diabetes mouse model and compared biochemical, histological and molecular parameters associated with kidney damage in Hif1alpha deficient (Hif1alpha (+/-) ) and wild-type mice. RESULTS: We showed that Hif1alpha deficiency accelerated pathological changes in the early stage of DN. Six weeks after diabetes-induction, Hif1alpha deficient mice showed more prominent changes in biochemical serum parameters associated with glomerular injury, increased expression of podocyte damage markers, and loss of podocytes compared to wild-type mice. These results indicate that Hif1alpha deficiency specifically affects podocyte survival in the early phase of DN, resulting in diabetic glomerular injury. In contrast, renal fibrosis was not affected by the global reduction of Hif1alpha, at least not in the early phase of diabetic exposure. CONCLUSIONS: Together our data reveal that HIF-1 has an essential role in the early response to prevent diabetes-induced tissue damage and that impaired HIF-1 signaling results in a faster progression of DN. Although the modulation of HIF-1 activity is a high-priority target for clinical treatments, further study is required to investigate HIF-1 as a potential therapeutic target for the treatment of DN. Twit Text FOAVip Renal injury is accelerated by global hypoxia-inducible factor 1 alpha deficiency in a mouse model of STZ-induced diabetes ????BMC Endocr Disord http://www.kidney.de/pget.php?&tw=1&pmid=28774305 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28774305 #FOAvip English Wikipedia <ref>{{Cite pmid|28774305}}</ref> Renal injury is accelerated by global hypoxia-inducible factor 1 alpha deficiency in a mouse model of STZ-induced diabetes #MMPMID28774305 Bohuslavova R; Cerychova R; Nepomucka K; Pavlinkova G BMC Endocr Disord 2017[Aug]; 17 (1): 48 PMID28774305show ga BACKGROUND: Hypoxia inducible factor 1 (HIF-1) activates protective pathways to counteract hypoxia and prevent tissue damage in conjunction with renal injury. The aim of this study was to evaluate a role of HIF-1 in diabetes-induced kidney damage. METHODS: We used a streptozotocin-induced diabetes mouse model and compared biochemical, histological and molecular parameters associated with kidney damage in Hif1alpha deficient (Hif1alpha (+/-) ) and wild-type mice. RESULTS: We showed that Hif1alpha deficiency accelerated pathological changes in the early stage of DN. Six weeks after diabetes-induction, Hif1alpha deficient mice showed more prominent changes in biochemical serum parameters associated with glomerular injury, increased expression of podocyte damage markers, and loss of podocytes compared to wild-type mice. These results indicate that Hif1alpha deficiency specifically affects podocyte survival in the early phase of DN, resulting in diabetic glomerular injury. In contrast, renal fibrosis was not affected by the global reduction of Hif1alpha, at least not in the early phase of diabetic exposure. CONCLUSIONS: Together our data reveal that HIF-1 has an essential role in the early response to prevent diabetes-induced tissue damage and that impaired HIF-1 signaling results in a faster progression of DN. Although the modulation of HIF-1 activity is a high-priority target for clinical treatments, further study is required to investigate HIF-1 as a potential therapeutic target for the treatment of DN. |*Disease Models, Animal[MESH] |Animals[MESH] |Diabetes Mellitus, Experimental/*complications/physiopathology[MESH] |Diabetic Nephropathies/*etiology/metabolism/pathology[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*deficiency/genetics[MESH] |Male[MESH] |Mice[MESH]Renal injury is accelerated by global hypoxia-inducible factor 1 alpha(epmc).pdf DeepDyve Pubget Overpricing