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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.

10.1038/srep17637 http://scihub22266oqcxt.onion/10.1038/srep17637 C4674698!4674698 !26656101     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26656101 &cmd=llinks): Failed to open stream: HTTP request failed! 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Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels |pdf=|usr=}}{{26656101 }} gab.com Text Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26656101 #FOAvip Injury to podocytes is considered a major contributor to diabetic kidney disease: their loss causes proteinuria and progressive glomerulosclerosis. Podocyte depletion may result from improper calcium handling due to abnormal activation of the calcium permeant TRPC (Transient Receptor Potential Canonical) channels. Angiotensin II (Ang II) levels are found to be elevated in diabetes; furthermore, it was reported that Ang II causes activation of TRPC6 in podocytes. We hypothesized here that Ang II-mediated calcium influx is aggravated in the podocytes under the conditions of type 1 diabetic nephropathy (DN). Diabetes was induced in the Dahl Salt-Sensitive rats by an injection of streptozotocin (STZ-SS). Eleven weeks post treatment was sufficient for the animals to develop hyperglycemia, excessive urination, weight loss, microalbuminuria, nephrinuria and display renal histological lesions typical for patients with DN. Patch-clamp electrophysiology performed on podocytes of the freshly isolated glomeruli showed enhanced basal TRPC channel activity in the STZ-SS rats, and increased response to Ang II; total calcium influx triggered by Ang II application was also augmented in podocytes of these rats. Our studies have a strong potential for advancing the understanding of TRPC-mediated effects on podocytopenia in DN initiation. Twit Text FOAVip Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26656101 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26656101 #FOAvip English Wikipedia <ref>{{Cite pmid|26656101 }}</ref> Podocyte injury in diabetic nephropathy: implications of angiotensin II-dependent activation of TRPC channels #MMPMID26656101 Ilatovskaya DV ; Levchenko V ; Lowing A ; Shuyskiy LS ; Palygin O ; Staruschenko A Sci Rep 2015[Dec]; 5 (ä): 17637 PMID26656101 show ga Injury to podocytes is considered a major contributor to diabetic kidney disease: their loss causes proteinuria and progressive glomerulosclerosis. Podocyte depletion may result from improper calcium handling due to abnormal activation of the calcium permeant TRPC (Transient Receptor Potential Canonical) channels. Angiotensin II (Ang II) levels are found to be elevated in diabetes; furthermore, it was reported that Ang II causes activation of TRPC6 in podocytes. We hypothesized here that Ang II-mediated calcium influx is aggravated in the podocytes under the conditions of type 1 diabetic nephropathy (DN). Diabetes was induced in the Dahl Salt-Sensitive rats by an injection of streptozotocin (STZ-SS). Eleven weeks post treatment was sufficient for the animals to develop hyperglycemia, excessive urination, weight loss, microalbuminuria, nephrinuria and display renal histological lesions typical for patients with DN. Patch-clamp electrophysiology performed on podocytes of the freshly isolated glomeruli showed enhanced basal TRPC channel activity in the STZ-SS rats, and increased response to Ang II; total calcium influx triggered by Ang II application was also augmented in podocytes of these rats. Our studies have a strong potential for advancing the understanding of TRPC-mediated effects on podocytopenia in DN initiation. |Albuminuria/etiology [MESH] |Angiotensin II/metabolism/pharmacology [MESH] |Animals [MESH] |Calcium/metabolism [MESH] |Diabetic Nephropathies/genetics/*metabolism/*pathology [MESH] |Disease Models, Animal [MESH] |Gene Expression [MESH] |Podocytes/drug effects/*metabolism/*pathology [MESH] |Rats [MESH] |Rats, Inbred Dahl [MESH]Podocyte injury in diabetic nephropathy: implications of angiotensin I(epmc).pdf DeepDyve Pubget Overpricing