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10.1038/srep45952 http://scihub22266oqcxt.onion/10.1038/srep45952 C5382679!5382679 !28383024     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28383024 &cmd=llinks): Failed to open stream: HTTP request failed! 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Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis |pdf=|usr=}}{{28383024 }} gab.com Text Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28383024 #FOAvip Salt-sensitive hypertension (SSHT) leads to kidney interstitial fibrosis. However, the potential mechanisms leading to renal fibrosis have not been well investigated. In present study, Dahl salt-sensitive (DS) rats were divided into three groups: normal salt diet (DSN), high salt diet (DSH) and high salt diet treated with hydrochlorothiazide (HCTZ) (DSH?+?HCTZ). A significant increase in systolic blood pressure (SBP) was observed 3 weeks after initiating the high salt diet, and marked histological alterations were observed in DSH rats. DSH rats showed obvious podocyte injury, peritubular capillary (PTC) loss, macrophage infiltration, and changes in apoptosis and cell proliferation. Moreover, Wnt/?-catenin signaling was significantly activated in DSH rats. However, HCTZ administration attenuated these changes with decreased SBP. In addition, increased renal and urinary Wnt4 expression was detected with time in DSH rats and was closely correlated with histopathological alterations. Furthermore, these alterations were also confirmed by clinical study. In conclusion, the present study provides novel insight into the mechanisms related to PTC loss, macrophage infiltration and Wnt/?-catenin signaling in SSHT-induced renal injury and fibrosis. Therefore, multi-target therapeutic strategies may be the most effective in preventing these pathological processes. Moreover, urinary Wnt4 may be a noninvasive biomarker for monitoring renal injury after hypertension. Twit Text FOAVip Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28383024 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28383024 #FOAvip English Wikipedia <ref>{{Cite pmid|28383024 }}</ref> Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induced Renal Injury and Interstitial Fibrosis #MMPMID28383024 Wei SY ; Wang YX ; Zhang QF ; Zhao SL ; Diao TT ; Li JS ; Qi WR ; He YX ; Guo XY ; Zhang MZ ; Chen JY ; Wang XT ; Wei QJ ; Wang Y ; Li B Sci Rep 2017[Apr]; 7 (ä): 45952 PMID28383024 show ga Salt-sensitive hypertension (SSHT) leads to kidney interstitial fibrosis. However, the potential mechanisms leading to renal fibrosis have not been well investigated. In present study, Dahl salt-sensitive (DS) rats were divided into three groups: normal salt diet (DSN), high salt diet (DSH) and high salt diet treated with hydrochlorothiazide (HCTZ) (DSH?+?HCTZ). A significant increase in systolic blood pressure (SBP) was observed 3 weeks after initiating the high salt diet, and marked histological alterations were observed in DSH rats. DSH rats showed obvious podocyte injury, peritubular capillary (PTC) loss, macrophage infiltration, and changes in apoptosis and cell proliferation. Moreover, Wnt/?-catenin signaling was significantly activated in DSH rats. However, HCTZ administration attenuated these changes with decreased SBP. In addition, increased renal and urinary Wnt4 expression was detected with time in DSH rats and was closely correlated with histopathological alterations. Furthermore, these alterations were also confirmed by clinical study. In conclusion, the present study provides novel insight into the mechanisms related to PTC loss, macrophage infiltration and Wnt/?-catenin signaling in SSHT-induced renal injury and fibrosis. Therefore, multi-target therapeutic strategies may be the most effective in preventing these pathological processes. Moreover, urinary Wnt4 may be a noninvasive biomarker for monitoring renal injury after hypertension. |Animals [MESH] |Antihypertensive Agents/pharmacology [MESH] |Blood Pressure/drug effects [MESH] |Capillaries/drug effects/metabolism [MESH] |Fibrosis/etiology [MESH] |Hydrochlorothiazide/pharmacology [MESH] |Hypertension/*complications/physiopathology/prevention & control [MESH] |Kidney Diseases/etiology/*pathology/prevention & control [MESH] |Kidney Tubules/blood supply/metabolism/pathology [MESH] |Kidney/drug effects/metabolism/*pathology [MESH] |Male [MESH] |Podocytes/drug effects/metabolism [MESH] |Rats, Inbred Dahl [MESH] |Sodium Chloride, Dietary/administration & dosage/toxicity [MESH]Multiple Mechanisms are Involved in Salt-Sensitive Hypertension-Induce(epmc).pdf DeepDyve Pubget Overpricing