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10.1161/JAHA.116.005092 http://scihub22266oqcxt.onion/10.1161/JAHA.116.005092 C5586267!5586267 !28673900     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28673900 &cmd=llinks): Failed to open stream: HTTP request failed! 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Inhibition of I?B Kinase at 24 Hours After Acute Kidney Injury Improves Recovery of Renal Function and Attenuates Fibrosis |pdf=|usr=}}{{28673900 }} gab.com Text Inhibition of I B Kinase at 24 Hours After Acute Kidney Injury Improves Recovery of Renal Function and Attenuates Fibrosis JO: J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=28673900 #FOAvip BACKGROUND: Acute kidney injury (AKI) is a major risk factor for the development of chronic kidney disease. Nuclear factor-?B is a nuclear transcription factor activated post-ischemia, responsible for the transcription of proinflammatory proteins. The role of nuclear factor-?B in the renal fibrosis post-AKI is unknown. METHODS AND RESULTS: We used a rat model of AKI caused by unilateral nephrectomy plus contralateral ischemia (30 minutes) and reperfusion injury (up to 28 days) to show impairment of renal function (peak: 24 hours), activation of nuclear factor-?B (peak: 48 hours), and fibrosis (28 days). In humans, AKI is diagnosed by a rise in serum creatinine. We have discovered that the I?B kinase inhibitor IKK16 (even when given at peak serum creatinine) still improved functional and structural recovery and reduced myofibroblast formation, macrophage infiltration, transforming growth factor-? expression, and Smad2/3 phosphorylation. AKI resulted in fibrosis within 28 days (Sirius red staining, expression of fibronectin), which was abolished by IKK16. To confirm the efficacy of IKK16 in a more severe model of fibrosis, animals were subject to 14 days of unilateral ureteral obstruction, resulting in tubulointerstitial fibrosis, myofibroblast formation, and macrophage infiltration, all of which were attenuated by IKK16. CONCLUSIONS: Inhibition of I?B kinase at peak creatinine improves functional recovery, reduces further injury, and prevents fibrosis. Twit Text FOAVip Inhibition of I B Kinase at 24 Hours After Acute Kidney Injury Improves Recovery of Renal Function and Attenuates Fibrosis ????J Am Heart Assoc http://www.kidney.de/pget.php?&tw=1&pmid=28673900 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28673900 #FOAvip English Wikipedia <ref>{{Cite pmid|28673900 }}</ref> Inhibition of I?B Kinase at 24 Hours After Acute Kidney Injury Improves Recovery of Renal Function and Attenuates Fibrosis #MMPMID28673900 Johnson FL ; Patel NSA ; Purvis GSD ; Chiazza F ; Chen J ; Sordi R ; Hache G ; Merezhko VV ; Collino M ; Yaqoob MM ; Thiemermann C J Am Heart Assoc 2017[Jul]; 6 (7 ): ä PMID28673900 show ga BACKGROUND: Acute kidney injury (AKI) is a major risk factor for the development of chronic kidney disease. Nuclear factor-?B is a nuclear transcription factor activated post-ischemia, responsible for the transcription of proinflammatory proteins. The role of nuclear factor-?B in the renal fibrosis post-AKI is unknown. METHODS AND RESULTS: We used a rat model of AKI caused by unilateral nephrectomy plus contralateral ischemia (30 minutes) and reperfusion injury (up to 28 days) to show impairment of renal function (peak: 24 hours), activation of nuclear factor-?B (peak: 48 hours), and fibrosis (28 days). In humans, AKI is diagnosed by a rise in serum creatinine. We have discovered that the I?B kinase inhibitor IKK16 (even when given at peak serum creatinine) still improved functional and structural recovery and reduced myofibroblast formation, macrophage infiltration, transforming growth factor-? expression, and Smad2/3 phosphorylation. AKI resulted in fibrosis within 28 days (Sirius red staining, expression of fibronectin), which was abolished by IKK16. To confirm the efficacy of IKK16 in a more severe model of fibrosis, animals were subject to 14 days of unilateral ureteral obstruction, resulting in tubulointerstitial fibrosis, myofibroblast formation, and macrophage infiltration, all of which were attenuated by IKK16. CONCLUSIONS: Inhibition of I?B kinase at peak creatinine improves functional recovery, reduces further injury, and prevents fibrosis. |Actins/metabolism [MESH] |Acute Kidney Injury/*drug therapy/enzymology/pathology/physiopathology [MESH] |Animals [MESH] |Antigens, CD/metabolism [MESH] |Antigens, Differentiation, Myelomonocytic/metabolism [MESH] |Creatinine/blood [MESH] |Disease Models, Animal [MESH] |Fibrosis [MESH] |I-kappa B Kinase/*antagonists & inhibitors/metabolism [MESH] |Kidney/*drug effects/enzymology/pathology/physiopathology [MESH] |Macrophages/drug effects/metabolism/pathology [MESH] |Male [MESH] |Myofibroblasts/drug effects/metabolism/pathology [MESH] |NF-kappa B/metabolism [MESH] |Protein Kinase Inhibitors/*pharmacology [MESH] |Rats, Wistar [MESH] |Signal Transduction/drug effects [MESH] |Smad2 Protein/metabolism [MESH] |Smad3 Protein/metabolism [MESH] |Time Factors [MESH]Inhibition of I?B Kinase at 24 Hours After Acute Kidney Injury Improve(epmc).pdf DeepDyve Pubget Overpricing